CoUege  of  ^{jpgiciansi  anb  ^urgeonst 
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Epidemic  Ceeebro-spinal  Meningitis 


AND    ITS    RELATION   TO 


Othee  Forms  of  Meningitis. 


LIBRARY 

OF  THE 

PATHOLOGICAL    LABORATORY, 

THE    PRESBYTERIAN    HOSPITAL, 

IN  THE  CITY  OF  NEW  YORK. 

A  REPORT 


State  Board  of  Health 


OF   aiASSACHUSETTS. 


BOSTON : 

WRIGHT   &   POTTER    PRINTING   CO.,  STATE  PRINTERS, 

18  Post  Office  Square. 

1898. 


LIBRARY 

OF  THE 

PATHOLOGICAL    LABORATORY, 

THE    PRESBYTERIAN    HOSPITAL, 

IN  THE  CITY  OF  NEW  YORK. 


TABLE  OF   CONTENTS. 


PAGE 

Preface, . 5 

History  of  the  Disease, 9 

Epidemic  Character  of  the  Disease, .  17 

Sporadic  Cases, 26 

Clinical  Cases, 30 

Bacteriology, 70 

Lumbar  Puncture, 79 

Gross  Pathological  Anatomy, 82 

Pathological  Histology, 101 

Classification  of  the  Disease, 125 

Symptomatology, 131 

Lesions  of  the  Eyes, 141 

Lesions  of  the  Ears,    ' 148 

Diagnosis, 161 

Summary, 162 

Other  Forms  of  Meningitis 165 

Pneumococcus  Meningitis, 166 

Streptococcus  Meningitis, 171 

Tubercular  Meningitis, 172 

Anthrax  Meningitis, 172 

Description  of  Plates, 174 

Bibliography 176 


UBRARY 

OF  THE 

PATHOLOGICAL    LABORATORY, 

THE    PRESBYTERIAN    HOSPITAL, 

IN  THE  CITY  OF  NEW  YORK. 


INTRODUCTORY. 


The  prevalence  of  epidemic  cerebro-spinal  meningitis  in 
Massachusetts  has  been  marked  with  much  irregularity.  An 
epidemic  of  unusual  severity  i5  1873  gave  rise  to  an  inves- 
tigation and  report  by  Dr.  J.  B.  Upham,  which  appeared 
in  the  report  of  the  State  Board  of  Health  for  that  year. 
A  summary  of  517  cases  reported  by  different  physicians 
throughout  the  State  was  given  in  that  report.  Dr.  Upham 
was  particularly  well  qualified  for  this  investigation  by  his 
previous  acquaintance  with  the  disease  in  Newbern,  North 
Carolina,  during  the  civil  war.  In  considering  the  causes 
of  the  disease  he  paid  particular  attention  to  the  influence 
of  insanitary  conditions  as  an  active  or  predisposing  cause. 
With  regard  to  this  he  says  :  — 

The  relation  of  insanitai'y  conditions  in  and  around  the  abode 
of  the  patient  to  its  origin  or  supposed  cause  demands  the  most 
careful  consideration.  In  weighing  the  evidence  contained  in  the 
returns,  I  find  the  scale  to  be  pretty  evenly  balanced  in  this  par- 
ticular. The  cases  are  distributed  among  all  classes  and  grades 
of  society,  —  the  high  and  low,  the  rich  and  the  poor,  locations 
unexceptionable  for  situation,  open  to  abundant  light  and  air, 
and  the  pent-up  hovels  of  the  lowly  and  wretched,  have  all  con- 
tributed to  the  material  of  the  epidemic.  We  believe,  therefore, 
that  the  primal  origin  of  the  disease  is  atmospheric,  and,  for  the 
present,  beyond  our  ken. 

Since  Dr.  Upham's  report,  great  discoveries  in  regard  to 
the  aetiology  of  many  of  the  infectious  diseases  have  been 
made.     The  bacterium  which  can  now  be  regarded  as  the 


Vlll 

essential  cause  of  epidemic  cerebro-spinal  meningitis  was 
discovered  in  1887,  but  the  first  important  confirmation  of 
that  discovery  was  not  made  until  1895.  There  has  always 
been  a  great  deal  of  obscurity  in  the  relations  between 
cerebro-spinal  meningitis  which  appeared  in  an  epidemic 
form  and  sporadic  cases  which  sometimes  appeared  alone 
or  in  connection  with  other  diseases,  and  which  were  very 
similar  in  their  clinical  manifestations  and  pathological 
lesions  to  the  epidemic  form.  With  the  view  of  clear- 
ing up  this  and  some  other  obscure  points  in  the  general 
aetiology  and  pathology  of  tke  disease,  the  present  inves- 
tigation has  been  undertaken  by  the  State  Board  of  Health. 
The  present  epidemic  is  the  only  one  of  considerable  impor- 
tance which  has  been  seen  since  the  advance  in  bacteriology 
and  pathology  has  made  such  an  investigation  possible.  In 
this  investigation  only  the  cases  which  were  seen  in  the 
principal  hospitals  and  in  which  the  diagnosis  of  the  disease 
could  be  regarded  as  certain  have  been  considered  at  any 
length. 

The  accuracy  of  the  statistics  relating  to  this  disease  must 
necessarily  be  questioned,  as  presenting  a  history  of  its  actual 
prevalence,  for  the  following  reason  :  — 

The  confusion  of  medical  terms  by  physicians,  together 
with  the  fact  that  all  returns  made  to  the  State  authorities 
are  copies  of  certificates,  and  not  originals,  and  that  these 
copies  are  in  the  majority  of  instances  made  by  men  who 
have  little  or  no  knowledge  of  the  significance  of  medical 
terms,  give  to  the  information  obtained  in  regard  to  this  dis- 
ease a  great  measure  of  uncertainty.  This  is  peculiarly  true 
of  epidemic  cerebro-spinal  meningitis,  —  a  disease  which  is 
liable  to  be  confounded  with  several  other  forms  of  brain 
disease,  in  consequence  of  the  similarity  in  nomenclature  of 
the  terms  employed  to  define  such  diseases.  In  addition  to 
this,  the  disease  is  not  a    common    one,    and   the    clinical 


IX 

manifestations  of  it  are  liable  to  be  confounded  either  with 
other  cerebral  diseases  or  with  forms  of  diseases  in  which 
cerebral  s^^mptoms  predominate. 

The  whole  number  of  deaths  reported  in  the  State  as  due 
to  cerebro-spinal  meningitis  during  the  period  of  nearly 
twenty  years,  ending  with  Oct.  1,  1897  (nineteen  years  and 
nine  months),  was  2,909,  or  nearly  150  per  year.  In  this 
summary  the  deaths  from  this  cause  in  the  fraction  of  the 
year  1897  are  those  which  were  reported  directly  to  the 
State  Board  of  Health  by  local  authorities.  The  numbers 
for  the  years  1878  to  1896,  inclusive,  were  fairly  uniform, 
the  maximum  being  171  in  1888  and  the  minimum  78  in 
1878.  But  in  the  first  nine  months  of  1897  the  number 
reported  to  the  State  Board  of  Health  was  405,  those  in 
Boston  alone  being  184. 

That  these  numbers  are  probably  much  too  large  is  shown 
by  a  classification  of  the  deaths  by  ages.  For  this  purpose 
the  deaths  occurring  in  the  nine  years,  1887-95,  are  selected, 
since  the  finer  distinction  of  separating  the  deaths  in  each  of 
the  first  five  years  of  life  was  first  introduced  into  the  State 
Kegistration  Eeport  in  1887.  The  deaths  recorded  in  those 
years  by  ages  were  as  follows  :  — 


Deaths  from  Cerebrospinal  Meningitis,  Massachusetts,  1887-95. 


AGE  PERIODS. 


0-1  year, 

1-2  years,     . 

2-3  years,     . 

3-4  years,     . 

4-5  years,     . 

5-10  years,  . 
10-15  years,  . 
15-20  3'ears,  . 
20-60  years,  . 
All  over  60  years, 

Totals,  . 


Deaths. 

Males. 

316 

180 

146 

74 

99 

51 

77 

41 

38 

19 

132 

59 

81 

47 

61 

36 

186 

89 

43 

12 

1,179 

608 

136 
72 
48 
36 
19 
73 
34 
25 
97 
31 


571 


By  the  foregoing  table  it  appears  that  316  deaths  from 
this  disease,  or  26 -\-  per  cent,  of  the  whole  number,  were 
reported  as  having  occurred  among  children  under  one 
year.  This  fact  necessarily  vitiates  the  accuracy  of  the 
returns  to  a  considerable  degree,  since  the  disease  is  ex- 
tremely rare  among  infants  as  well  as  among  those  of  ad- 
vanced years. 

The  reported  deaths  from  this  cause  occurred  mainly  in 
the  large  cities  and  towns,  the  whole  number  reported 
from  towns  of  less  than  5,000  inhabitants  being  only  136, 
or  less  than  5  per  cent,  of  the  whole  number. 

The  map  of  Boston  which  faces  the  title  page  of  this 
monograph  presents  the  locality  of  those  cases  only  which 
were  treated  at  certain  hospitals  of  Boston  during  the 
spring  of  1897.  A  similar  map  could  not  have  been 
prepared  with  accuracy  for  the  State,  for  the  reason,  as 
already  stated,  that  very  many  cases  reported  in  towns 
and  cities  elsewhere  and  not  under  hospital  supervision 
were  not  genuine  cases  of  this  disease. 


Epidemic  Cerebeo-spinal  Meningitis 


AND  ITS  RELATION  TO 


Othee  Foems  of  Meningitis. 


EPIDEMIC  CEREBRO-SPIML  MEXIXGITIS  AXT)  ITS 
EELATION  TO  OTHER  EOEMS  OE  MENINGITIS. 


PREFACE. 


We  shall  endeavor  in  tbis  paper  to  describe  the  epidemic  of 
cerebro-spinal  meningitis  which  has  prevailed  in  this  community 
during  the  past  winter  and  spring,  aud  also  to  consider  other 
forms  of  meningitis  allied  to  the  epidemic  form.  The  disease 
has  a  peculiar  interest  here,  from  the  fact  that  in  the  United 
States  it  was  first  recognized  as  an  independent  disease  in 
Medfield,  Mass.,  a  year  after  the  appearance  of  the  disease 
in  Geneva,  by  Danielson  and  Mann,^'^*  whose  observations 
were  made  independently  of  those  of  Vieusseaux^*  in  Geneva. 
In  the  epidemic  at  the  beginning  of  the  century  the  disease 
was  more  prevalent  in  the  New  England  States  than  elsewhere 
in  this  country,  and  in  subsequent  epidemics  there  have  been 
many  cases   in   these    States. 

The  literature  of  the  disease  has  been  enriched  by  the  care» 
ful  studies  of  these  epidemics  in  New  England.  The  clear 
objective  description  of  the  character  of  the  disease  by  Daniel- 
son  and  Mann,  with  the  records  of  autopsies,  served,  as  much 
as  the  somewhat  earlier  description  of  Vieusseaux,  to  establish 
the  disease  as  an  entity.  The  most  complete  of  the  earlier 
descriptions  is  contained  in  the  report  of  a  committee  of  the 
Massachusetts  Medical  Society,  appointed  in  1809  to  investigate 
the  disease.  The  secretary  of  the  committee  and  the  author 
of  the  report  was  James  Jackson. ^^  The  committee  carefully 
investigated  the  symptoms  and  course  of  the  disease,  its  relation 
to    other   diseases,  its    pathology  and   most   approved    mode    of 

•  The  small  numbers  refer  to  the  bibliography. 


6 

treatment.  The  report  contains  the  records  of  eight  post- 
mortem examinations,  made  by  J.  C.  Warren/^^  one  of  the 
members  of  the  committee.  Another  report  on  the  disease, 
which  is  one  of  the  classics  in  medicine,  is  that  of  Elisha 
North^^  of  Goshen,  Conn.,  in  1811.  In  a  small  book,  now 
very  rare,  he  gives  the  result  of  his  own  observations,  together 
with  reports  from  others,  both  physicians  and  laymen,  which 
appeared  in  the  various  newspapers  of  the  day.  A  committee 
appointed  by  the  Massachusetts  Medical  Society  made  a  report 
on  the  epidemic  which  appeared  in  this  State  in  1864  and 
1865.^®  In  reference  to  the  same  epidemic  a  Boylston  prize 
essay  by  Dr.  S.  G.  Webber^^  gives  the  best  account  which 
has  ever  appeared  of  the  history  of  the  disease  and  its  relation 
to  other  epidemics.  In  this  paper  Dr.  Webber  takes  the 
ground  that  the  disease  is  probably  identical  with  some  of 
the  earlier  and  imperfectly  described  epidemics  of  Europe. 
It  is  to  be  regretted  that  this  paper  of  Dr.  Webber's,  which 
aj)peared  in  the  form  of  a  long  serial  in  the  "  Boston  Medical 
and  Surgical  Journal,"  should  have  so  generally  escaped  the 
notice  of  subsequent  writers.  There  is  further  a  careful  study 
of  the  epidemic  of  1874  by  Upham,"*^  who  had  previously 
become  acquainted  with  the  disease  in  Newbern,  N.  C,  during 
the  civil  war.  We  should  have  some  hesitation  in  adding 
to  the  voluminous  literature  of  the  disease,  were  it  not  for 
the  fact  that  the  recent  advances  in  the  technique  of 
investigation,  and  the  possibility,  which  the  discovery  of  the 
organism  of  the  disease  has  given  us,  of  studying  the 
lesions  and  symptoms  in  relation  with  the  setiological 
factor,  have  enabled  us  to  fill  out  some  points  only  touched 
upon   by  the   earlier   investigators. 

We  wish  to  express  our  deep  indebtedness  to  the  physicians 
of  the  City  Hospital,  the  Massachusetts  General  Hospital  and 
the  Children's  Hospital,  who  have  generously  placed  their 
clinical  observations  and  cases  at  our  disposal.  Our  work  has 
been  further  materially  assisted  by  the  zeal  and  enthusiasm 
of  the  assistants  in  the  laboratories  of  the  City  and  Massa- 
chusetts  General   hospitals. 


"We  are  indebted  to  Dr.  Wentwortb  for  bis  notes  on  spinal 
puncture,  witb  descriptions  of  tbe  cbaracter  of  tbe  fluid  witb- 
drawn.  Dr.  Edwin  Jack  bas  allowed  us  to  publish  bis 
observations  on  tbe  cbaracter  of  tbe  eye  complications  of  tbe 
disease  wbicb  be  observed  at  tbe  Cbildren's  Hospital. 

Tbe  plates  wbicb  accompany  tbe  article  with  one  exception 
are  from  water-color  paintings  made  by  Miss  Byrnes.  Tbey 
were  drawn  by  tbe  camera  lucid  a,  with  little  or  no  assistance 
from  tbe  autbors,  and  represent  actual  conditions. 

Under  tbe  term  meningitis  is  understood  inflammation  of  the 
pia-aracbnoid,  tbe  membrane  wbicb  forms  tbe  immediate  invest- 
ment of  tbe  brain  and  spinal  cord.  Tbe  separation  of  tbis  mem- 
brane into  tbe  pia  and  arachnoid  is  artificial,  although  there  is  more 
justification  for  such  a  separation  in  tbe  spinal  cord  than  in  the 
brain.  Considered  as  a  single  membrane,  it  consists  of  a  serous 
surface  (arachnoid)  in  contact  with  the  dura,  forming  one  side  of 
the  sub-dural  space,  and  beneath  tbis  a  loose  connective  tissue  (pia 
mater)  containing  numerous  and  large  lymph  spaces  and  carrying 
the  blood  vessels  for  tbe  brain  and  cord.  In  tbe  spinal  cord  there 
is  a  single  large  space  between  tbe  upper  serous  surface  and  the 
tissue  which  closely  invests  the  cord,  crossed  by  numerous  fibrous 
trabeculse.  The  lymph  spaces  in  the  membrane  communicate  with 
the  lymph  sheaths  around  tbe  vessels  of  the  brain  and  cord,  and 
by  means  of  the  lymphatics  accompanying  the  nerves,  with  the 
general  lymphatic  system  of  tbe  body.  The  membrane  in  the  form 
of  tbe  choroid  plexus  passes  into  the  ventricles  of  the  brain. 

The  surface  forming  part  of  the  sub-dural  space  is  covered  with 
a  single  layer  of  endothelial  cells  ;  beneath  this  there  is  a  more  or 
less  definite  layer  of  connective  tissue,  which  passes  into  tbe  loose 
connective  tissue  of  the  pia  with  its  numerous  lymph  spaces  and 
blood  vessels.  This  tissue  contains  the  single  connective  tissue 
cells  of  the  fibrous  tissue,  tbe  cells  of  tbe  blood  vessels  and  lym- 
phatics, and  a  variable  number  of  lymphoid  cells  which  are  found 
in  the  lymphatics   and  in  the  lymph  spaces  around  the  vessels. 

There  are  various  means  by  which  infectious  agents  can  gain 
access  to  this  tissue.  Tbey  may  enter  into  it  by  means  of  the 
blood  or  by  the  extension  of  infectious  processes  from  adjacent 


8 

regions.  The  extension  may  be  direct,  or  by  means  of  lym- 
phatics which  communicate  directly  or  indirectly  with  those  of 
the  membrane. 

All  inflammatory  processes  in  the  pia-arachnoid,  however  pro- 
duced, agree  more  or  less  in  their  anatomical  features ;  and  in  so 
far  as  the  symptoms  depend  upon  the  purely  local  lesions,  there  is 
considerable  uniformity  in  the  symptoms  produced.  There  are, 
however,  certain  minor  differences  in  the  anatomical  lesions  which 
are  sufficient  to  differentiate  certain  forms  of  meningitis  from 
others.  These  differences  depend  in  general  upon  the  extent  and 
character  of  the  exudation,  upon  the  varying  degree  in  which  the 
blood  vessels  and  nerves  are  involved,  and  upon  the  direct  exten- 
sion of  the  process  in  the  meninges  into  the  adjacent  tissues  of  the 
brain  and  cord.  In  some  cases  the  lesions  are  limited  to  the  mem- 
branes ;  in  others  there  is  a  tendency  for  the  process  to  extend  into 
the  adjacent  nervous  tissue  and  along  the  nerves.  There  is  little 
doubt  that  all  cases  of  meningitis  are  cerebro-spinal,  the  meninges 
of  the  cord  being  affected  as  well  as  those  of  the  brain.  The  cord 
lesions  are,  however,  so  much  more  marked  in  certain  cases  that 
these  have  been  especially  distinguished  by  the  name  cerebro- 
spinal meningitis. 

In  epidemic  cerebro-spinal  meningitis  there  are  sufficient  differ- 
ences in  the  character  of  the  exudation,  in  the  greater  degree  of 
involvement  of  the  meninges  of  the  cord,  in  the  extension  of  the 
inflammation  along  the  nerves,  and  in  the  participation  of  the 
tissue  of  the  brain  and  cord  in  the  process,  to  enable  us  to  dis- 
tinguish anatomically  most  cases  of  this  from  other  forms  of 
meningitis.  There  is  a  further  difference  between  the  epidemic 
cerebro-spinal  meningitis  and  all  other  forms  of  meningitis,  in 
the  general  absence  of  inflammatory  lesions  in  the  intima  of 
the  arteries  in  the  epidemic  variety,  while  it  is  common  in  all 
the   other   forms. 

The  peculiarity  of  all  lesions  produced  by  the  tubercle  bacillus 
enables  us  to  distinguish  tuberculous  meningitis  from  the  other 
forms.  There  are  few  differences  between  the  inflammations  pro- 
duced by  the  streptococcus,  the  staphylococcus  aureus  and  the 
diplococcus   lanceolatus.     There    are   certain    peculiarities  in  the 


9 

anatomical  processes  in  all  forms  of  meningitis  which  are  depend- 
ent upon  the  character  of  the  tissue  affected.  Inflammations  of 
the  meninges  due  to  the  action  of  certain  organisms  differ  some- 
what from  the  lesions  produced  by  the  same  organisms  elsewhere 
in  the  body.  Tuberculosis  of  the  membrane  appears  both  in  the 
form  of  tubercle  formation  along  the  vessels,  and  as  a  diffuse 
inflammation  due  to  a  fibrino-purulent  exudation ;  the  latter  may 
be  present  to  such  an  extent  that  the  tubercles  may  be  overlooked. 
In  all  forms  of  meningitis  the  inflammatory  exudation  is  more 
marked  on  the  base  than  over  the  convexity  of  the  brain,  and 
along  the  posterior  than  the  anterior  surface  of  the  cord. 


EPIDEMIC  CEREBRO-SPINAL  MENINGITIS. 

It  is  usually  considered  that  epidemic  cerebro-spinal  meningitis 
first  appeared  in  1805  in  G-eneva.  Vieusseaux"^  described  an 
uncommon  disease  which  appeared  in  Geneva  in  the  winter  and 
spring  of  1805.  The  disease  commenced  suddenly  with  loss 
of  strength,  vomiting,  violent  pains  in  head  and  along  spine, 
and,  in  infants,  with  convulsions.  The  course  of  the  disease 
was  rapid  in  fatal  cases,  lasting  from  twelve  hours  to  five 
days.  In  the  greater  number  of  patients  who  died  in  twenty- 
four  hours  the  body  was  covered  with  violet  spots. 

Mathey"^  gives  an  account  of  a  post-mortem  examination  made 
of  one  of  the  fatal  cases.  He  describes  a  gelatinous  exudation 
covering  the  convex  surface  of  the  brain,  and  a  yellow  puri- 
form  matter  upon  its  posterior  aspect,  upon  the  optic  commis- 
sure, and  the  inferior  surface  of  the  cerebellum  and  the  medulla 
oblongata.  The  description  of  Vieusseaux  combined  with  the 
post-mortem  examination  described  by  Mathey  can  leave  no 
doubt  as  to  the  character  of  the  disease. 

Although  this  is  generally  regarded  as  the  beginning  of  epidemic 
cerebro-spinal  meningitis,  there  can  be  little  doubt  that  the  disease 
existed  previously.  Among  the  early  accounts  of  epidemics  sim- 
ilar to  cerebro-spinal  meningitis,  Bascome,^  in  his  history  of 
"  Epidemic  Pestilences,"  speaks  of  a  local  epidemic  at  Roettinggen 
in  Franconia  in  the  autumn  of    1802,    in  which  the  young  and 


10 

strong  were  suddenly  seized  U^ith  pain  and  anguish  at  the  heart 
and  pain  in  the  nape  of  the  neck.  In  the  fatal  cases  the  patient 
fainted,  the  limbs  became  rigid,  and  death  sometimes  took  place 
twenty-four  hours  from  the  commencement  of  the  attack.  It  is 
interesting,  as  showing  the  probably  greater  distribution  of  the 
disease,  to  note  that  in  the  same  volume  of  the  "  Medical  and 
Agricultural  Register"  which  contains  the  description  of  Danielson 
and  Mann  there  is  a  letter  from  Indiana,  describing  a  severe 
epidemic  which  appeared  there  in  Vincennes.  The  disease 
especially  affected  young  females,  and  some  of  the  symptoms 
would  point  to  meningitis.  The  editor  of  the  magazine  very  per- 
tinently asks  if  this  be  not  the  same  disease  described  by  Daniel- 
son  and  Mann.  In  the  histories  of  the  great  epidemics  of  Europe, 
from  the  thirteenth  century  on,  symptoms  are  described  which 
almost  certainly  point  to  this  disease.  A  very  interesting  account 
of  these  early  epidemics  and  their  affinity  to  or  identity  with 
cerebro-spinal  meningitis  is  given  by  Webber  in  his  admirable 
account  of  the  history  of  the  disease.  The  descriptions  of 
these  epidemics  are  exceedingly  obscure,  and,  in  the  general 
absence  of  the  records  of  post-mortem  examinations,  it  is  im- 
possible to  say  exactly  what  disease  they  represent.  The  descrip- 
tions of  the  clinical  symptoms  could  apply  equally  to  typhus, 
typhoid  or  cerebro-spinal  meningitis.  Webber  attaches  consider- 
able importance  to  the  description  of  the  skin  lesions,  but  these 
are  not  sufficiently  constant  or  sufficiently  characteristic  to  serve 
as  a  means  of  diagnosis. 

In  his  work  on  the  diseases  of  the  army,  published  in  1752, 
Sir  John  PringalP"  gives  an  account  of  a  jail  or  hospital 
fever,  which  in  many  respects  was  similar  to  cerebro-spinal 
meningitis.  On  post-mortem  examination  suppuration  of  the 
brain  was  found. 

The  classification  of  a  disease  should  always  be  made  from 
an  astiological  point  of  view ;  the  recognition  of  a  definite  in- 
fectious agent  establishes  the  identity  of  a  disease.  In  the 
absence  of  this,  a  definite  class  of  symptoms,  based  on  certain 
anatomical  lesions,  is  our  only  method  of  classification.  The 
insufficiency  of  this  method  of  classification  is  shown  by  the  fact 


11 

that  before  the  recognition  of  the  infectious  agent  causing  epi- 
demic cerebro-spinal  meningitis  there  was  no  way  of  separating 
sporadic  cases  and  small  epidemics  of  this  disease  from  menin- 
gitis caused  by  other  infectious  agents. 

After  the  epidemic  at  Geneva  the  disease  next  appeared  in 
Medfield,  Mass.,  and  was  described  by  Danielson  and  Mann  in 
1806.  The  publication  of  Danielson  and  Mann  was  made  in- 
dependently of  the  work  of  Vieusseaux,  with  which  they  were 
not  familiar.  They  described  carefully  the  symptoms  of  the 
disease,  and  gave  the  results  of  five  post-mortem  examinations. 
They  speak  particularly  of  the  uniformity  of  the  symptoms  and 
the  mode  of  attack.  The  disease  soon  became  rapidly  diffused 
in  the  New  England  States.  It  extended  to  nearly  all  the  towns 
in  Massachusetts,  and  was  particularly  severe  in  "Worcester ; 
then  it  appeared  in  New  Hampshire,  Connecticut,  New  York, 
New  Jersey,  Vermont  and  Maine,  and  kept  up  continuously  in 
one  place  or  another  in  New  England  until  1816. 

There  are  two  classical  descriptions  of  the  epidemic  of  this 
period.  One  is  by  Elisha  North"^  and  the  other  by  a'  com- 
mittee appointed  by  the  Massachusetts  Medical  Society^"^'  to 
investigate  the  new  disease.  The  committee  was  composed  of 
Drs.  James  Jackson,  J.  C.  Warren  and  Thos.  "Welch,  and  the 
report  was  written  by  James  Jackson,  the  secretary.  The  com- 
mittee sent  letters  to  various  physicians  all  over  the  State,  and 
analyzed  their  replies.  The  disease  was  described  as  beginning 
suddenly  with  great  prostration,  intense  pai-i  in  the  head  and 
along  the  spine,  and  vomiting.  Many  of  the  cases  died  sud- 
denly in  ten  to  twelve  hours ;  others  in  twenty-four  to  forty- 
eight  hours  after  the  first  symptoms.  Almost  all  the  fatal 
cases  died  before  the  third  day.  The  disease  affected  espe- 
cially young  persons  of  both  sexes,  but  not  generally  very 
young  infants  or  aged  persons.  The  committee  reported  in 
all  eight  autopsies,  most  of  which  were  made  by  J.  C.  "Warren. 

Jackson  thinks  that  the  description  of  malignant  fever  by  Sen- 
nert^^  agrees  in  many  respects  with  this  disease.  He  thinks  the 
seat  of  the  disease  is  not  in  the  skin  lesions  but  in  the  mem- 
branes of  the  brain,  the  skin  lesions  being  secondary  and  symp- 


12 

tomatic.  Notwithstanding  the  infrequency  of  the  skin  lesions 
and  their  varying  character,  the  disease  continued  to  be  named 
petechial  or  spotted  fever. 

North  describes  the  disease  from  his  personal  experience  with 
it,  and  appends  to  this  various  other  accounts  which  have  been 
given  by  contemporaneous  authors.  North  divided  the  disease 
into  two  types  depending  on  the  more  or  less  rapid  course  of 
the  disease  and  the  intensity  of  the  symptoms. 

Dr.  Samuel  Woodward,^^  in  a  newspaper  printed  in  Hartford, 
describes  an  epidemic  in  Litchfield  County  in  1807.  In  the 
same  paper,  Dr.  Bestor,  after  giving  an  excellent  account  of 
the  clinical  course  of  the  disease,  says  that,  though  it  has  been 
attributed  to  various  causes,  he  is  convinced  that  the  "immediate 
cause  of  the  disease  is  the  increase  in  the  sensorial  power  of  sen- 
sation with  the  decrease  of  the  sensorial  power  of  irritation."  The 
book  of  North  also  contains  a  description  of  the  disease  by  Dr. 
Fiske,  "  Sketch  of  Spotted  Fever"  ("Massachusetts  Spy,"  April 
9,  1810),  "  Observations  on  Anomalous  and  Irregular  Diseases," 
by  Dr.  Williamson  (Baltimore,  1808 ;  letter  to  Philadelphia  Med- 
ical Museum),  and  a  collective  report  from  Drs.  Haskel,  Spooner 
and  Holmes,  who  were  a  committee  appointed  at  Farmington, 
Conn.,  to  investigate  the  disease. 

Hirsch^"  divides  the  history  of  the  disease  into  four  periods. 
The  first,  from  1805  to  1830,  shows  the  disease  in  isolated  epidem 
ics  in  various  places  in  Europe,  but  more  generally  in  the  United 
States.  In  the  second  period,  from  1837  to  1850,  the  disease 
became  prevalent  in  wide-spread  epidemics  in  France,  Italy, 
Algiers,  the  United  States  and  Denmark.  During  the  third  period, 
from  1854  to  1875,  it  reached  its  widest  diffusion  throughout  most 
of  Europe,  the  adjoining  countries  of  Asia,  the  United  States  and 
some  parts  of  Africa  and  South  America.  The  fourth  period,  from 
1876  to  the  present  day,  shows  a  return  in  slight  epidemics  of  more 
or  less  considerable  groups  of  cases  in  various  countries,  but  par- 
ticularly in  the  United  States,  Germany  and  Italy.  In  this  last 
period  there  has  been  very  little  of  the  disease  in  France.  In  the 
first  period  it  was  seen  in  Canada  in  1807  ;  in  Virginia,  Kentucky 
and  Ohio,  in  1808  ;  in  New  York  and  Pennsylvania,  the  year  after. 


13 

The  year  1816  forms  the  close  of  these  series  of  epidemics,  with 
the  exception  of  one  at  Middletown,  Conn.,  in  1823,  and  one  at 
TrnmbuU,  O.,  in  1828.  The  United  States  was  free  from  epidemic 
cerebro-spinal  meningitis  until  the  year  1842.  In  Europe  in  the 
first  period  there  was  an  epidemic  in  Paris  in  1814,^^^  in  1815  at 
Metz,^*^  and  in  subsequent  years  in  two  or  more  villages  in  the 
province  of  Geneva,  and  in  a  few  places  in  Germany. 

Lichtenstern*^^  gives  Sibergundi^^  the  credit  for  the  first  descrip- 
tion of  the  disease  in  Westphalia,  Germany.  In  the  second 
period,  from  1837  to  1850,  the  disease  first  broke  out  in  two 
localities  in  the  south  of  France^  in  Bayonne  and  the  department 
of  the  Landers  on  one  hand,  and  the  districts  of  Foix  and 
Narbonne  on  the  other.  It  extended  all  over  France,  most  of 
the  cases  being  among  the  garrisons,  and  next  to  France  its 
greatest  ravages  were  in  southern  Italy.  The  only  other  country 
in  Europe  in  which  meningitis  was  prevalent  to  any  extent  during 
this  period  was  Denmark,  and  from  here  it  was  probably  carried 
to  Iceland.  In  Germany  there  are  references  to  a  few  slight  epi- 
demics of  encephalitis  and  acute  hydrocephalus,  which  in  all 
probability  were  cerebro-spinal  meningitis.  In  the  United  States 
in  this  period  the  disease  appeared  principally  in  small  epi- 
demics in  the  western  and  southern  States.  The  most  extensive 
epidemic  was  seen  at  New  Orleans,  in  a  regiment  of  recruits 
which  had  come  there  from  Mississippi.  In  1848  it  was  seen 
in  the  towns  of  Millbury  and  Sutton,  in  Worcester  County, 
Mass.,  and  described  by  Sargent. ^^ 

The  second  period  was  characterized  chiefly  by  the  prevalence 
of  the  disease  among  the  troops.  The  epidemic  was  most 
prevalent  in  France,  and  in  nearly  all  cases  it  appeared  first 
in  the  military,  and  from  there  in  some  cases,  notably  in  Metz, 
extended  to  the  civil  population. 

The  descriptions  of  the  disease  by  French  authorities  during  this 
time  are  of  great  value.  They  devoted  their  attention  chiefly  to 
the  description  of  the  course  of  the  disease,  the  rare  symptoms, 
the  manifold  complications,  the  ordinary  and  the  rarer  pathologi- 
cal lesions.  The  most  prominent  of  the  French  treatises  are 
those  of  Rollet,^-^*^  Tourdes,^^''  Forget^^^  and  Broussais.^^^ 


14 

In  the  third  period  the  disease  began  in  Sweden,  a  country 
hitherto  free  from  it,  and  prevailed  there  in  extensive  epidemics 
for  ten  years  (Hirsch) .  Another  one  of  its  principal  seats  was 
Germany,  where  it  reached  its  height  in  1864  and  1865. 
Here  it  first  appeared  in  Silesia,  and  broke  out  almost  simul- 
taneously at  a  number  of  points  in  east  and  west  Prussia, 
gradually  extending  throughout  south  Germany. 

In  this  period  the  best  descriptions  are  those  of  Wunderlich^*' 
of  the  disease  in  Leipzig,  and  of  Ziemsen  and  Hess^*^  of  the 
epidemic  in  Erlangen.  The  disease  appeared  in  Berlin  in  1864, 
and  the  pathological  lesions  were  carefully  described  by  Klebs,^* 
who  reported  the  results  of  twenty-six  autopsies.  Kotsonopulos^^ 
described  an  epidemic  of  the  disease  in  Nauplia,  Greece,  in  1869, 
and  in  1873  he  gave  a  further  account,  showing  that  the  epi- 
demic of  1869  continued  with  a  number  of  single  cases  and 
small  epidemics  until  1873. 

The  United  States  was  free  from  the  disease  from  1850  to 
1857,  when  it  again  appeared  in  two  such  widely  separated 
areas  as  North  Carolina'^^^  and  the  western  part  of  New  York.^^ 
During  the  civil  war,  from  1861  to  1864,  the  disease  became 
widely  spread.  In  the  winter  of  1861  and  1862  it  appeared 
in  the  Army  of  the  Potomac  and  in  camp  near  Washington,"^ 
and  was  especially  severe  among  the  negroes  sent  by  the 
Confederates  to  Memphis. 

Upham"''  gives  an  account  of  the  disease  as  it  appeared  in 
the  winter  and  spring  of  1862  and  1863  in  the  camps  in  and 
around  Newbern,  N.  C.  He  compares  the  symptoms  observed 
in  this  epidemic  with  those  of  the  Massachusetts  epidemic  in 
1810,  and  concludes  that  both  diseases  were  the  same.  He 
made  a  number  of  post-mortem  examinations,  and  gives  a 
careful  description  of  the  anatomical  lesions. 

The  disease  appeared  again  in  Massachusetts  in  1864  and 
1865,  and  a  report  was  made  on  it  in  1865  by  a  committee 
appointed  by  the  Massachusetts  Medical  Society.  The  report 
of  this  committee,  unlike  that  of  1810,  did  not  make  any 
material  addition  to  our  knowledge  of  the  disease.  The  disease 
was  also   described    at   this   time    by  Webber,  whose    article   is 


15 

chiefly  valuable  for  his  study  of  the  history  of  the  disease  and 
the  relations  of  early  epidemics  to  it. 

From  1865  there  was  a  period  of  quiescence  in  Massachusetts 
until  1872  and  1873,  when  there  was  another  severe  epidemic  in 
Boston,  which  was  reported  by  Upham."*'  In  Philadelphia  and 
other    parts    of    Pennsylvania    there   was    a   severe    epidemic   in 

1863,  which  was  described  by  Stille."^ 

The  disease  took  the  character  of  a  very  wide-spread  epidemic 
in  Ireland  in  the  first  half  of  the  year  1866,  appearing  in  Dublin 
and  the  surrounding  country.  It  was  spoken  of  by  the  people  as 
the  "  black  death."  It  appeared  first  among  the  troops,  and 
extended  from  these  to  the  civic  population,  being  most  prominent 
among  the  troops  in  1866  and  among  the  population  in  1867. 

From  1860  to  1874  epidemics  of  the  disease  were  seen  in  almost 
all  parts  of  the  United  States.  The  epidemics  usually  appeared  in 
the  winter  and  reached  the  greatest  extension  in  the  spring. 
Hirsch  thinks  that  in  the  last  period,  beginning  in  1876,  the 
disease  is  retreating  into  narrower  limits,  so  that  it  nowhere 
retains  a  character  of  a  prevalent  disease  of  the  people.  A  review 
of  the  literature  since  1884,  the  date  of  the  publication  of  his 
work,  shows  numerous,  for  the  most  part  small,  epidemics,  in 
widely  different  localities.  In  this  period  also  reports  of  a  great 
many  sporadic  cases  of  the  disease  have  been  published.  The 
reports  of  so  many  sporadic  cases  are  probably  due  in  part  to 
the  closer  observation  and  better  recognition  of  the  disease,  and 
the  greater  interest  which  the  development  of  our  knowledge  of 
bacteria  has  brought  about.  In  1876  there  was  a  small  epi- 
demic at  Birmingham,  reported  by  Forster^*^  and  at  Galston 
near  Glasgow,  reported  by  Frew.^ 

Striimpel,^^  in  an  article  on  "  Pathology  of  Cerebro-spinal 
Meningitis,"  says  that  the  disease  has  continued  in  Leipzig  since 

1864,  a  few  cases  being  seen  every  year.  In  the  first  half  of 
the  year  1879,  at  the  same  time  with  the  extensive  epidemic  of 
recurrent  fever,  the  disease  became  more  common  and  prevailed 
to  a  slight  extent  up  to  the  summer  of  1880.  In  1881  he  saw 
four  cases.  Frolik-*^  reports  a  small  epidemic  in  the  garrison  in 
Leipzig.      The    disease    began   to    appear    in    1877,   and    up    to 


16 

October,  1879,  sixteen  cases  were  taken  to  the  hospital,  of  which 
five  died  and  eleven  recovered.  Leyden''^  says  there  has  been 
in  recent  years  slight  epidemics  of  the  disease  in  Berlin,  espe- 
cially in  the  year  1885  and  the  spring  of  1886.  Bliimm^  re- 
ports a  small  epidemic  in  Sulzbach,  and  says  that  at  the  same 
time  single  cases  or  small  epidemics  were  observed  in  the 
surrounding  towns.  In  Ziemssen's  clinic  in  Munich  in  1890 
there  were  seventeen  cases  and  three  deaths,  and  in  the  clinic 
of  Bauer  in  the  same  city  there  were  twenty-four  cases  and 
eight  deaths.  > 

Leichtenstern^^  gives  an  account  of  cerebro-spinal  meningitis 
on  the  Rhine  from  1885  to  1893.  The  disease  appeared  in 
Cologne  in  1885,  and  reached  an  epidemic  extension.  One  hun- 
dred and  eleven  cases  occurred,  with  thirty-seven  deaths.  There 
were  thirty-four  cases  in  1886,  twenty-six  in  1888,  and  in  other 
years  a  varying  small  number  of  cases. 

In  1890  the  disease  extended  from  Cologne  to  the  neighboring 
village  of  Diisseldorf,  where  there  was  a  small  epidemic  of  twenty 
cases  with  six  deaths.  Panienski^  reports  a  small  epidemic  in 
Karlsruhe  in  the  winter  of  1892  and  1893,  in  which  there  were 
sixteen  cases  and  seven  deaths.  A  small  epidemic  of  thirty 
cases  appeared  in  Copenhagen  in  1891,  which  was  described  by 
Friis.-^  Austria  has  generally  been  more  or  less  free  from  the 
disease. 

Karg"''  reports  a  small  epidemic  in  the  Orphanage  of  Vienna 
in  1863.  Warschauer^^^  reports  an  epidemic  in  Cracow,  which 
prevailed  principally  among  the  Jews,  whom  he  considers  more 
susceptible  to  the  disease  than  the  Slavonic  population.  In 
1867  Baxa^  describes  an  extensive  epidemic  which  prevailed  in 
Pola  in  Bohemia.  One  hundred  and  twenty-nine  cases  occurred, 
with  a  mortality  of  sixty-six  per  cent.  In  1868  a  similar  epi- 
demic prevailed  at  the  same  place.  At  various  other  places  in 
the  Austrian  monarchy  there  are  reports  of  small  scattered  epi- 
demics, none  of  them  reaching  any  considerable  extent.  In  the 
United  States  since  1876  sporadic  cases  and  small  epidemics  have 
been  seen  in  various  places.  The  most  extensive  epidemics  dur- 
ing this  period  have  been  those  of  New  York^  in  1893,  that  in 


17 

Lanaconing,  McL,  in  the  same  year,  and  the  recent  epidemic 
in  Boston,  1896  and  1897.  Many  of  the  epidemics  have  not 
embraced  more  than  four  to  six  cases,  and  most  of  the  accounts 
concern  only  sporadic  cases. 

The  Character  of  the  Epidemic. 

Considered  as  an  epidemic,  cerebro-spinal  meningitis  has  many 
features  which  distinguish  it  from  epidemics  of  the  other  infectious 
diseases.  As  a  rule,  none  of  the  epidemics  has  shown  a  con- 
tinuous extension,  this  being  noticeably  the  case  with  the  first 
recognized  epidemics.  After  the  disease  had  appeared  in  Geneva 
in  1805  its  next  appearance  was  in  Medfield,  Mass.,  and  shortly 
after  this  it  appeared  in  other  towns  in  New  England,  Illinois, 
New  York,  New  Jersey  and  Maryland.  In  some  cases,  as  in  the 
French  epidemics  from  1840  lo  1845,  it  appeared  to  extend  with 
the  movements  of  the  troops.  It  was  undoubtedly  carried  into 
Algiers  in  this  period  by  the  French  troops.  In  almost  all  cases 
it  appeared  first  among  the  troops,  and  from  these  it  extended  to 
the  civic  population.  Hirsch,  in  his  study  of  the  disease,  has 
found  only  one  instance  in  which  an  epidemic  has  followed  a  regu- 
lar course.  In  the  diffusion  of  the  disease  through  central  Fran- 
conia  it  travelled  somewhat  regularly  from  north-east  to  south-west. 
As  a  rule,  the  outbreaks  of  the  disease  have  been  seen  as  perfectly 
isolated  epidemics  in  places  which  had  been  hitherto  free  from  it. 

Almost  all  of  the  epidemics  have  appeared  in  the  winter  and 
spring.  Vieusseaux  pointed  out  that  the  disease  in  Geneva  dis- 
appeared on  the  approach  of  mild  spring  weather.  All  of  the 
early  epidemics  in  Massachusetts  were  seen  in  the  winter  and 
spring.  "Woodward  speaks  of  the  disease  in  Litchfield  County 
appearing  in  April,  when  the  frost  was  dissolving  and  the  ground 
breaking  up,  and  says  the  disease  seemed  to  be  more  common  in 
rainy  weather. 

Love"^  has  pointed  out  that  the  epidemic  in  New  Orleans  in 
the  winter  of  1847  was  confined  to  one  regiment  newly  arrived 
from  Mississippi,  who  were  quartered  in  bad  barracks,  on  damp 
ground,  and  exposed  in  their  wet  clothes  to  the  cold.  Other 
troops  quartered  near  them,  which  were  seasoned  to  the  weather 


18 


and  supplied  with  woollen  clothing,  remained  absolutely  free  from 
the  disease. 

Baxa^  shows  that  the  epidemic  in  Pola  commenced  in  January 
and  lasted  until  the  end  of  May.  There  were  no  cases  in  the 
summer,  and  in  1868  the  disease  broke  out  again.  Although 
the  disease  frequently  begins  in  the  winter,  it  usually  reaches  its 
height  in  the  spring  months,  April  and  May. 

In  the  epidemic  in  New  York,  both  in  1892  and  1893  the 
greatest  number  of  cases  was  found  in  May.  In  the  epidemic 
of  Cologne,  in  1885,  the  greatest  number  of  cases  was  seen  in 
April,  although  there  were  but  slight  differences  in  May  and 
June.  In  the  Strassburg  epidemic  among  the  soldiers  in  1841 
the  greatest  number  of  cases  was  seen  in  March,  there  being 
in  that  one  month  sixty-five  out  of  a  total  of  one  hundred  and 
ninety-eight  cases. 

Hirsch  reports  a  few  exceptions  to  this  general  rule.  At  Bor- 
deaux, 1839,  Toulouse,  1842,  Dublin,  1850,  and  Chrzanow,  1874, 
the  disease  first  appeared  in  the  summer.  The  weather  in  itself 
probably  has  little  to  do  with  the  disease,  because  the  number  of 
cases  has  frequently  increased  with  the  approach  of  warm  spring 
weather  and  an  increase  in  the  temperature. 

This  supposed  relation  between  the  period  of  the  year  and  the 
appearance  of  the  epidemic  led  people  to  suppose  that  cold  in 
itself  could  be  an  exciting  cause.  Lowy^  says  cold  and  heat, 
rain  and  sunshine  have  nothing  to  do  with  the  appearance  and 
extension  of  the  epidemics. 

Table  I. 


Jan. 

Feb. 

March 

April 

May 

June 

July 

Aug. 

Bept. 

Get. 

Nov. 

1896,    ,     . 

- 

- 

- 

•       - 

- 

1 

- 

- 

1 

- 

- 

1897,    .     . 

1 

10 

23 

29 

21 

14 

7 

0 

3 

- 

- 

Dec. 


The  preceding  table  gives  the  date  of  the  appearance  of  the 
disease  in  the  cases  observed  in  the  hospitals  of  Boston  in  the 
present  epidemic.  From  this  it  will  be  seen  that  the  greatest 
number  of  cases  was  in  the  spring  months.     The  first  case  seen 


19 


■was  in  June,  but  the  epidemic  character  of  the  disease  was  not 
recognized  until  the  following  February. 

Age. 
In  general  the  disease  has  been  most  prevalent  in  children 
and  young  adults.  The  cases  occurring  in  the  military  epi- 
demics were  mostly  young  soldiers,  from  the  age  of  eighteen  to 
twenty-four  years.  Leichtenstern  found,  in  the  epidemic  in  Cologne 
in  1885,  out  of  one  hundred  and  eleven  cases,  only  twenty- 
three  which  occurred  after  the  thirtieth  year.  More  than  half 
of  his  cases  occurred  before  twenty-one.  The  following  table, 
taken  from  Leichtenstern,  gives  the  ages  of  cases  seen  in  the 
epidemic  in  1885,  and  in  the  small  epidemics  which  followed 
this. 

Table  II. 


rt 

e 

n 

e 

m 

9 

m 

e 

w 

e 

ifl 

e 

to 

, 

e 

w( 

et 

« 

M 

M 

* 

* 

w 

la 

e 

e 

*>i 

w^ 

« 

H 

IS 

>« 

«S 

w* 

e 

w( 

n 

pN 

« 

o 

o 

"* 

9 

rt 

FK 

« 

« 

M 

M 

■* 

e 

Iffl 

19 

e 

« 

t' 

H 

1885, 

17 

14 

10 

19 

18 

10 

6 

6 

4 

1 

1 

4 

- 

1 

- 

111 

1886, 

- 

3 

3 

11 

7 

2 

1 

2 

1 

2 

1 

1 

- 

- 

- 

34 

1887, 

- 

2 

1 

- 

- 

- 

- 

- 

1 

- 

- 

- 

- 

- 

- 

4 

1888, 

2 

2 

1 

7 

9 

3 

- 

2 

- 

- 

- 

- 

- 

- 

- 

26 

1889, 

- 

- 

1 

1 

1 

- 

- 

1 

- 

- 

- 

- 

1 

- 

- 

5 

1890, 

- 

- 

1 

- 

- 

1 

- 

- 

- 

- 

- 

- 

1 

- 

1 

4 

1891, 

1 

- 

- 

1 

1 

1 

- 

- 

- 

- 

- 

- 

- 

- 

4 

1892, 

2 

- 

- 

3 

1 

- 

- 

- 

- 

- 

- 

- 

- 

- 

- 

6 

Totals, 

22 

21 

17 

42 

37 

17 

7 

11 

6 

3 

2 

5 

2 

1 

1 

194 

Of  twenty-eight  cases  reported  by  Rollet,^^^  sixteen  were  from 
eighteen  to  twenty-two  years,  eleven  from  twenty-three  to 
twenty-seven  years,  and  only  a  single  case  of  thirty  years. 
The  cases  seen  by  him  extended  from  January  to  August. 

Striimpel™  observed  thirty-two  cases,  twenty-four  of  which  were 
between  ten  and  thirty  years.  The  youngest  case  was  in  a  child 
four  and  one-half  months  ;  the  two  oldest  cases  were  fifty-two  and 
sixty-six  years. 


20 


The  epidemics  in  the  early  part  of  the  century  were  particu- 
larly prevalent  in  children.  At  more  advanced  periods  of  life 
meningitis  is  very  rare. 

The  following  table  gives  the  ages  of  the  cases  seen  in  the 
present  epidemic.  Only  those  cases  which  were  seen  in  the  hos- 
pitals are  considered.  A  separate  tabulation  of  those  under  five 
years  of  age  shows  but  five  .cases  under  three  years  and  one 
under  one  year.  Nothing  shows  the  inaccuracy  of  mortality 
tables  of  cerebro-spinal  meningitis  more  than  the  analysis  of 
ages  in  the  cases  in  which  diagnosis  is  certain.  Epidemic 
cerebro-spinal  meningitis  is  exceedingly  rare  under  one  year 
of  age.  All  other  forms  of  meningitis,  though  rare  at  this  age, 
are  more  common  than  the  epidemic.  In  mortality  statistics  of 
the  disease  a  large  percentage  of  cases  is  put  down  as  under 
one  year.  In  the  present  epidemic  no  cases  were  seen  in  the 
infant  hospital. 

Table  III. 


e 

10 

S 

m 

e 

iffl 

e 

10 

© 

rt 

© 

« 

LO 

wH 

1-1 

w 

w 

M 

M 

^ 

"K 

rt 

ffl 

© 

© 

e 

w4 

e 

p4 

(S 

pH 

<c 

J^ 

e 

M 

© 

© 

I"l 

m 

W 

M 

M 

M 

* 

* 

US 

w 

18 

12 

6 

11 

16 

20 

13 

s 

1 

3 

1 

2 

0 

There  is  a  general  agreement  among  writers  on  the  disease  as  to 
contagion.  Vieusseaux"*  says  the  extension  of  the  disease  shows 
that  it  is  not  contagious.  In  G-eneva  it  began  among  the  poor 
population,  living  generally  under  bad  hygenic  conditions,  and  did 
not  extend  from  case  to  case.  The  attendants  on  the  sick  and  the 
neighbors  remained  free  from  it.  Even  when  there  were  two  sick 
in  the  same  house,  the  disease  usually  appeared  at  the  same  time, 
and  they  did  not  acquire  it  from  one  another. 

North''^  says,  in  speaking  of  the  epidemic  character  of  the  dis- 
ease :  "I  have  known  more  than  one  instance  in  which  persons 
coming  from  a  part  of  the  country  where  the  epidemic  has  never 
prevailed,  and  resting  a  short  time  in  a  town  where  the  disorder 
has  been  epidemic,  have  had  the  disease  at  a  season  when  the 
inhabitants  of  the  said  town  had  been  free  from  it.     I  have  also 


21 

known  persons  who  resided  in  sections  of  the  country  where  this 
epidemic  appeared,  after  having  been  on  a  journey  to  places 
where  it  had  never  been,  attacked  with  it  soon  after  returning 
home,  and  at  a  season  when  it  did  not  attack  those  in  different 
circumstances." 

Stevenson  and  Smith^"''  reported  a  small  epidemic  in  Davonport 
in  1885.  The  first  cases  were  seen  on  some  ships  moored  there, 
and  then  the  troops  in  the  barracks  became  infected  without 
there  having  been  any  communication  between  the  ships  and  the 
troops. 

Berg,^  in  the  epidemic  in  New  York  in  1893,  could  not  find  a 
single  case  in  which  two  or  more  members  of  the  same  family  were 
affected.  The  outbreaks  occurred  in  widely  separated  parts  of  the 
city,  and  no  relation  could  be  traced  between  the  various  outbreaks. 

Panienski**  reports  an  epidemic  in  Carlsruhe.  The  disease 
began  among  the  soldiers,  and  after  a  number  of  cases  had 
occurred  a  portion  of  the  garrison  which  had  not  been  affected 
were  sent  to  Rastatt.  One  of  the  men  in  the  garrison  there  was 
affected  the  next  day,  and  then  after  a  pause  of  four  weeks 
there  were  three  other  cases,  all  of  which  recovered.  In  the 
town  of  Carlsruhe  there  were  sixteen  cases.  Coleman^^"  gives 
the  following  observations  on  contagiousness :  — 

No.  1.  Man,  aged  sixty-one  years,  typical  case  of  the  disease.  In; 
the  same  house  several  weeks  later  the  eighteen-year-old  son  became 
affected,  and  one  week  later  the  daughter. 

No.  2.  Fourteen-year-old  boy  died  with  typical  disease.  His  mother 
became  attacked  with  croupous  pneumonia,  which  was  followed  two 
days  afterwards  by  meningitis.. 

No.  3.  Girl,  seventeen  years,  died  with  typical  disease,  Body  re- 
mained in  the  house  four  days.  Clothes  from  the  house  were  lent  tO' 
other  people,  among  whom  several  cases  of  the  disease  appeared. 

Herman  and  Kober^^  in  reporting  the  epidemic  of  cerebro- 
spinal meningitis  in  upper  Sicilia,  in  Beuthen,  say  that  the 
epidemic  was  not  limited  to  a  definite  place,  but  broke  out  in 
a  number  of  places,  most  cases  coming  from  crowded  and  filthy 
parts  of  the  city.  Several  cases  appeared  in  the  same  house  or 
room.    No  infections  were  observed  in  the  hospitals. 


22 

Singer^''^  reported  in  tbe  epidemic  in  Tirgul  Frumor  that  eight 
members  of  the  same  family  died  of  the  disease.  Baxa^  found 
in  one  house  four  deaths,  in  another  three,  in  three  others  two. 

Friis,^  in  the  epidemic  in  Copenhagen,  1891,  found  that  the 
disease  generally  occurred  in  small  family  or  house  epidemics  of 
from  two  to  five  cases. 

Peterson*''  studied  the  epidemic  which  prevailed  in  Berlin  in 
1895  and  1896,  and  thinks  that  infection  takes  place  by  per- 
sonal contact  or  by  visiting  infected  localities.  The  disease 
may  be  given  to  children  by  intermediate  conveyors  who  remain 
healthy. 

Gahlberg,^  in  the  epidemic  in  Mailberg,  found  there  were 
numerous  cases  from  the  same  house,  and  the  disease  was 
especially  virulent  in  certain  streets. 

Nowlin^^^  found  in  the  small  epidemic  of  five  cases  of  Shelby- 
ville,  Tenn.,  that  two  cases  arose  in  the  same  house. 

Leichtenstern'^^  has  collected  the  cases  bearing  on  contagion 
in  the  epidemic  studied  by  him.  In  this  epidemic  there  was  a 
small  house-epidemic  in  the  hospital,  in  which  four  nurses  on  the 
medical  side  of  the  house,  four  employees  of  the  house  who  in  no 
way  came  in  contact  with  the  sick,  and  one  patient  who  was  care- 
fully isolated  in  the  syphilitic  division,  became  affected.  In  one 
hundred  and  eighty  cases  in  which  the  dwelling  could  be  ascer- 
tained, one  hundred  and  fifty  came  each  from  one  house. 

In  the  Strassburg  epidemic,  in  1840,  the  disease  appeared 
among  the  soldiers  in  October.  The  first  case  in  the  civic  popula- 
tion appeared  in  January,  1841.  Hirsch^^  gives  the  following 
interesting  observations  :  — 

On  the  8th  of  February,  "  K,"  twenty  years  old,  in  Sczakan,  became 
infected  with  meningitis,  and  was  cared  for  by  a  woman  from  Sullen- 
cyen.  After  the  death  of  "  K,"  "  W,"  who  had  cared  for  him,  returned 
to  Sullencyen  and  died  there  of  meningitis  on  the  26th  of  February.  A 
family,  "  K,"  accompanied  by  the  boy  "  D  "  and  the  four-year-old  daugh- 
ter of  a  teacher,  "  O,"  came  to  the  funeral  of  this  girl.  Shortly  after  the 
return  to  Podgass  a  small  child  of  the  family  "  K,"  the  boy  "  D  "  and  the 
daughter  "  O  "  all  died  of  the  disease. 

Herman'*^  gives  a  case  of  house  infection  in  the  epidemic  in 
Breslau  in  1887.     A  family  in  which  there  had  been  meningitis 


23 

moved  from  a  house  and  another  family  moved  into  it.  In  this 
family  there  were  several  cases.  He  thinks  that  the  epidemic 
in  1887  was  a  continuation  of  the  one  in  1879,  there  being 
sporadic  cases  between  the  two  epidemics. 

In  the  epidemic  in  Beuthen,  reported  by  Richter/^^  there  were 
fifty-six  cases  and  twenty-four  deaths.  Seventeen  of  the  cases 
came  from  tap  rooms,  and  he  thinks  that  in  such  localities  there 
may  be  foci  of  infection. 

Richter^^  thinks  that  the  disease  may  be  contagious.  He  often 
found  cases  in  the  same  family,  and  the  disease  spread  most  in 
places  where  people  congregated.  He  gives  one  case  which 
speaks  strongly  for  contagion.  A  woman  visited  at  a  house 
where  two  children  had  been  sick  with  the  disease  ;  she  stayed 
in  the  house  one  day,  and  then  visited  an  uncle.  She  had 
meningitis  on  the  fourth  day.  In  the  last  days  of  her  disease, 
on  November  6,  she  was  visited  by  a  young  man;  on  the  10th 
he  had  a  light  case  ;  after  five  days  he  returned  to  his  business, 
and  on  the  19th  an  apprentice  in  the  same  shop  was  affected. 
The  period  of  incubation  he  thought  was  about  five  days. 

In  a  question  of  the  probability  of  transmission  of  an  in- 
fectious disease  we  should  consider  the  location  of  the  disease 
and  the  ways  in  which  the  organism  causing  it  can  pass  from 
the  lesions  of  the  disease  to  the  outside  ;  further,  the  viability 
of  the  organisms  and  their  possibility  of  leading  a  saprophytic 
existence.  The  lesions  of  meningitis  are  chiefly  in  the  meninges 
of  the  brain  and  cord,  and  confined  to  these  organs  in  most  cases. 
While  located  in  the  meninges,  there  is  little  or  no  opportunity 
for  the  organism  to  infect  the  outside.  In  a  certain  number  of 
cases  there  are  lesions  in  the  lungs,  ears  and  nose,  in  which 
large  numbers  of  organisms  are  present,  and  from  which  an 
infection  of  neighboring  objects  or  persons  could  easily  take 
place.  The  organism,  as  far  as  we  have  been  able  to  tell 
from  its  behavior  in  culture  media  and  in  the  tissues,  has  a 
feeble  vitality,  and  would  not  be  capable  of  leading  a  sapro- 
phytic existence.  In  the  report  on  the  bacteriology  of  the  dis- 
ease will  be  found  some  observations  bearing  on  the  vitality  of 
the   organism   producing   it,    when  subjected  in  pure  culture   to 


21 

various  external  conditions.  Still,  it  must  be  remembered  that 
we  cannot  reproduce  artificially  all  the  conditions  which  organ- 
isms might  find  in  nature.  It  is  certain  that  the  disease  is  an 
infectious  disease,  and  is  produced  by  a  definite  micro-organism. 
This  organism  increases  in  the  body  of  the  affected  individual, 
and  in  a  certain  number  of  cases  may  infect  his  surroundings, 
and  may  in  a  manner  which  we  do  not  know  be  conveyed  to 
the  tissues  of  a  susceptible  individual  and  there  produce  the 
disease.  Why  this  takes  place  in  some  cases  and  not  in  others, 
and  the  conditions  under  which  it  takes  place,  we  do  not  know. 
The  evidence,  on  the  whole,  is  not  conclusive  that  the  disease 
is  incapable  of  being  transmitted  from  one  individual  to  another. 
In  the  present  epidemic  there  were  but  few  cases  in  which  sev- 
eral individuals  in  the  same  house  were  affected.  In  one  case 
a  mother  was  attacked  two  days  after  the  death  of  her  child 
from  the  fulminating  form.  In  two  other  cases  there  were 
cases  in  the  same  family,  and  in  one  case  it  was  said  that 
children  in  the  same  neighborhood  had  died  of  brain  fever. 

We  have  been  able  to  find  but  little  in  the  literature  bearing 
on  the  subject  of  immunity  in  this  disease.  North,^^  in  his  de- 
scription of  individual  cases,  gives  one  undoubted  case  in  which 
there  was  an  attack  twenty-five  months  previously.  Another 
case  had  the  disease  in  August,  1808,  and  was  again  attacked 
in  May,  1810.  Herman  and  Kober^  report  that  a  girl  who  had 
the  disease  in  May,  1886,  died  in  the  second  epidemic  the  fol- 
lowing year.  Lowy^  reports  a  second  attack  three  weeks  after 
apparent  recovery.  Warshauer"^  reports  a  case  in  a  woman 
who  had  the  disease  in  an  epidemic  five  years  previously. 
From  the  fact  that  second  '  attacks  are  so  rarely  mentioned,  it 
would  appear  that  a  relatively  high  degree  of  immunity  must 
be  conferred  by  a  single  attack.  In  the  present  epidemic  there 
was  no  history  of  a  previous  attack. 

Hygienic  conditions  do  not  appear  to  play  much  part  in  influ- 
encing the  epidemics.  Randolph  found,  in  the  epidemic  in  Lana- 
coning,  that  virulent  types  of  the  disease  appeared  in  such  widely 
different  localities  and  under  such  different  hygienic  conditions 
that  he  thinks  that  hygienic  conditions  can  have  but  little  to  do 


25 

with  the  extension  of  the  disease.  Claverie,^^  in  the  epidemic 
observed  in  Rocheford,  found  that  the  disease  was  not  more 
prevalent  in  the  crowded  parts  of  the  city.  In  Barden  the  dis- 
ease seemed  to  shun  the  most  crowded  streets  and  only  appeared 
in  the  best  streets.  He  quotes  Laveran  as  saying. that  the  dis- 
ease once  appeared  in  the  barracks  when  very  few  troops  were 
in  them,  and  disappeared  when  they  filled  up  again.  The  re- 
ports of  most  epidemics  show  that  the  disease  is  more  prevalent 
in  the  poorer  and  more  crowded  parts  of  the  cities.  The  map 
at  the  end  shows  the  distribution  of  the  cases  in  this  city 
which  came  to  the  hospitals.  It  is  seen  from  this  that  with 
the  exception  of  a  small  area  along  the  water  front,  the  cases 
were  pretty  equally  distributed  over  the  city. 

Rollet^'^  gives  the  mortality  in  all  the  epidemics  in  France  up 
to  1844.  At  Nancy,  where  Rollet  observed  his  cases,  the  mor- 
tality was  28  per  cent.  ;  Le  Mans,  33^  per  cent. ;  Ancenis,  33^ 
per  cent.  ;  Montbrison,  34  per  cent. ;  Caen,  40  per  cent.  ;  Poi- 
tiers, 40  per  cent.  ;  Versailles,  48  per  cent. ;  Metz,  55  per  cent.  ; 
Perpignan,  56  per  cent.  ;  Strassburg  Military  Hospital,  58  per 
cent. ;  Strassburg,  inhabitants,  60  per  cent. ;  Laval,  63  per  cent.  ; 
Colmar,  71  per  cent.  ;  Bayonne,  75  per  cent.  ;  Aigues-Mortes,  75 
per  cent.  General  average  of  all  cases,  51  per  cent.  The  mor- 
tality varies  greatly  in  different  epidemics.  Hirsch'^^  gives  it  as 
from  20  to  75  per  cent.  In  this  epidemic  one  hundred  and  eleven 
cases  were  seen  in  the  three  hospitals.  Of  these,  seventy-six  died 
and  thirty-five  recovered,  a  mortality  of  68|^  per  cent. 

With  the  view  of  ascertg.ining  the  prevalence  of  the  disease  in 
the  State,  the  following  circular  letter  was  sent  to  three  hundred 
and  fifty  physicians  :  — 

COMMONWEALTH    OF    MASSACHUSETTS. 

State  Board  of  Health, 
State  HorsE,  Boston,  Mass.,  Sept.  1,  1897. 

Dear  Doctor  :  —  During  the  past  year  an  epidemic  of  cerebro-spinal 
meningitis  has  prevailed  in  Massachusetts,  a  large  number  of  cases 
having  been  seen  in  the  hospitals  of  Boston.  With  the  view  of  ascer- 
taining the  extent  of  the  epidemic  and  the  prevalence  of  the  disease  in 
private  practice,  the  following  circular  letter  has  been  addressed  to  a 
number  of  physicians  :  — 


26 

1.  Have  you  seen  any  cases  of  epidemic  cerebro-spinal  meningitis  in  your  practice 

in  1896  or  1897  ?     (If  the  cases  were  seen  in  Boston,  give  their  residence, 
street  and^number.) 

2.  Under  what  form  of  the  disease  did  these  cases  come  ? 

3.  Among  what  class  of  the  population  did  such  cases  arise  ? 

4.  Were  you  led  to  believe  that  the  disease  is  communicable  ? 

5.  "What  was  the  mortality  ? 

6.  Were  autopies  made,  and  result  ? 

Remarks :  — 

One  hundred  and  fifty  replies  were  received  from  physicians 
in  all  of  the  large  cities  and  a  number  of  the  towns.  Positive 
reports,  in  most  cases  giving  short  and  adequate  clinical  his- 
tories, were  received  from  twenty-one  physicians.  Cases  of 
the  disease  were  reported  in  Springfield,  Gardner,  Marlborough, 
Framingham,  Lowell,  Lexington,  Weston,  Tewksbury,  Waltham, 
Newton,  Melrose,  Somerville,  Gloucester,  Rockland,  Cambridge 
and  Quincy.  With  the  exception  of  Springfield,  where  one 
case  was  reported,  and  Gardner,  where  two  cases  were  reported, 
all  of  the  reports  come  from  towns  within  a  radius  of  thirty 
miles  of  Boston.  With  the  exception  of  Rockland  and  Quincy, 
all  are  to  the  west  of  or  north  of  the  city.  Of  course  a 
number  of  cases  reported  in  the  practice  of  single  physicians 
represent  but  a  small  fraction  of  the  total  number  of  cases 
which  may  have  occurred.  It  is  seen  from  this  that  the  epi- 
demic was  not  confined  to  Boston,  but  that  cases  occurred  in 
other  parts  of  the  State. 

Sporadic  Cases. 

The  accounts  given  of  epidemics  of  cerebro-spinal  meningitis 
show  that  they  are  not  of  short  duration.  In  the  table  given  by 
Leichtenstern^^  (Table  II.)  he  shows  the  number  of  cases  which 
were  observed  in  Cologne  from  1885-92.  It  will  be  seen  from 
this  that  in  1887,  1889,  1890,  1891  and  1892  there  was  a  small 
number  of  cases  each  year,  and  in  1888  a  larger  number.  The 
epidemics  appear  in  many  cases  to  have  been  preceded  and  fol- 
lowed by  a  number  of  sporadic  cases. 

Striimpel,"^  in  1882,  says  that,  since  the  appearance  of  the  dis- 
ease in  Leipzig  in  1863  and  1864,  single  cases  have  been  seen 
almost  every  year,  but  they  never  rose  to  an  epidemic  extension 


27 

until  the  first  half  of  the  year  1879.  At  that  time  and  with  the 
epidemic  of  recurrent  fever  the  disease  became  more  frequent,  and 
in  the  months  from  April  to  June  thirteen  cases  were  taken  into 
the  hospital.  Then  the  epidemic  extended  in  small  numbers  until 
the  summer  of  the  following  year,  during  which  time  fifteen  more 
cases  were  taken  in  ;  finally,  after  a  still  longer  pause  in  February 
and  March  of  1881,  four  cases  were  received.  Leyden,"^  in  1887, 
says  that  sporadic  cases  have  still  remained  after  the  great  epi- 
demic in  1864  and  1865.  In  recent  years  there  have  been  slighter 
epidemics  in  Berlin,  embracing  a  considerable  number  of  cases. 
This  was  especially  in  the  year  1885  and  in  the  spring  of  1886, 
when  there  were  several  cases.  Mason*^^  reports  five  cases  of 
cerebro-spinal  meningitis  occurring  from  18S1  to  1883  in  Boston, 
and  says  there  has  been  a  steady  decline  in  the  number  of  cases  of 
this  disease  since  1874,  but  a  small  number  are  seen  in  every  part 
of  the  State  except  on  Cape  Cod.  Herman  and  Kober^  say  that 
sporadic  cases  have  been  observed  in  the  years  preceding  the  epi- 
demic extension. 

These  reports  as  to  the  sporadic  cases,  coming  from  observers 
who  are  well  acquainted  with  the  epidemic  form,  are  interesting. 
Omerod^^  reports  ten  cases  of  sporadic  meningitis,  with  autopsies. 
Four  of  these  cases  occurred  between  March  and  June,  1890,  and 
in  the  summer  of  the  same  year  there  was  an  epidemic  of  the 
disease  in  the  eastern  counties  of  P^ngland.  He  thinks  that  the 
sporadic  cases  do  not  differ  from  the  epidemic  cases.  In  all  of 
Omerod's  cases  the  cord  was  examined  and  spinal  meningitis 
found.  They  all  had  the  same  clinical  history,  and  the  same  con- 
ditions were  found  at  autopsy,  as  in  the  epidemic  cases.  Both  the 
clinical  and  the  gross  anatomical  descriptions  of  Omerod  are 
excellent,  and  it  is  greatly  to  be  regretted  that  they  were  not  com- 
pleted by  bacteriological  cultures.  Osler^  reports  a  case  of  spo- 
radic meningitis  of  a  chronic  form,  which  was  followed  by  total 
blindness  which  was  gradually  recovered  from.  Rotch,"^  in  an 
article  on  meningitis,  in  his  text-book  gives  an  admirable  pict- 
ure of  a  chronic  case  of  sporadic  meningitis,  with  recovery, 
which  would  seem  almost  certainly  to  have  been  the  epidemic 
form.     Senator^"^  reports  a  case  of  sporadic  meningitis  in  which 


28 

the  clinical  history  conforms  exactly  to  the  type  of  the  chronic 
epidemic  disease.  The  disease  lasted  from  May  13  to  August 
8,  and  was  characterized  by  great  emaciation. 

Sinclair  also  reports  a  case  of  sporadic  meningitis  in  the  Dundee 
Royal  Infirmary.  Both  from  the  clinical  history  and  the  autopsy 
this  seems  to  have  been  of  the  epidemic  form,  and  there  were  no 
other  cases  of  meningitis  in  the  vicinity  at  that  time. 

May,  Schmidt  and  Kastner^^  reported  twenty-four  cases  of 
sporadic  cerebro-spinal  meningitis  from  the  clinic  of  Professor 
Bauer  between  1885  and  1889.  There  was  acute  swelling  of  the 
spleen  in  eight  cases.  It  is  probable  that  many  of  these  cases 
represent  sporadic  cases  of  the  epidemic  form,  but  in  the  absence 
of  bacteriological  examinations  it  must  remain  uncertain.  The 
same  may  be  said  of  the  seventeen  cases  reported  from  Ziemmsen's 
clinic  in  the  same  period. *  The  comparatively  small  mortality 
would  show  that  the  cases  were  of  the  epidemic  form.  In  Bauer's 
cases  there  were  eight  deaths  out  of  twenty-four,  and  in  Ziemm- 
sen's three  out  of  seventeen.  Senator^"^  reports  several  sporadic 
cases  in  Berlin  in  1886,  with  two  autopsies.  Reichmann^^^  gives  a 
number  of  sporadic  cases  in  which  the  symptoms  were  in  all 
respects  similar  to  the  epidemic  form.  One  case  lasted  from  the 
5th  of  June  to  the  14th  of  August.  Laboulene®*  says  that  most  of 
the  epidemics  have  left  in  their  trail  sporadic  cases  analogous  to 
Asiatic  cholera.  There  is  but  one  report  of  a  case  of  sporadic 
meningitis  in  which  the  diplococcus  intracellularis  was  found  ; 
this  is  by  Stoeltzner,  who  found  these  organisms  in  a  typical 
sporadic  case. 

In  going  over  the  literature  of  the  disease  we  find  a  great  many 
reports  of  sporadic  cases,  some  of  them  of  single,  others  of 
multiple  cases.  Of  course  it  is  very  difficult  to  say  whether  these 
cases  were  of  the  epidemic  form  or  some  one  of  the  other  forms. 
Neither  the  clinical  history  nor  the  autopsy  without  cultures  are 
absolutely  conclusive.  In  going  over  the  clinical  histories  of 
large  numbers  of  cases  one  receives  an  impression  of  the  epi- 
demic form  which  differs  somewhat  from  that  of  the  pneumo- 
coccus  form  and  the  streptococcus  form,  but  the  clinical  history 


29 

alone  is  not  conclusive.  Autopsy  accounts  would  be  more  con- 
clusive had  they  been  accompanied  with  cultures  or  even  with 
careful  histological  investigations.  The  importance  of  combined 
clinical  and  pathological  investigation  is  very  evident  in  going 
over  these  reports.  There  are  careful  clinical  histories  given  with 
imperfect  accounts  of  autopsies  and  without  bacteriological  investi- 
gation, and  in  those  cases  in  which  the  latter  were  carried  out  the 
clinical  histories  were  either  absent  altogether  or  very  meagre.  In 
the  reports  of  these  sporadic  cases  it  may  be  generally  assumed 
that  the  recoveries  were  of  the  epidemic  form.  So  far  we  have 
not  been  able  to  find  a  case  which  certainly  could  be  regarded, 
from  the  accompanying  pneumonia  or  endocarditis,  as  pneumococ- 
cus  meningitis,  which  has  recovered.  Of  course  there  is  a  certain 
number  of  cases  of  pneumococcus  meningitis  in  which  the  affection 
of  the  meninges  is  primary,  and  it  is  impossible  to  say  with  regard 
to  these  cases  whether  there  are  any  recoveries  among  them.  In 
the  same  way  there  are  no  recoveries  noted  from  cases  of  menin- 
gitis secondary  to  thrombosis  of  the  lateral  sinuses  or  disease  of 
the  middle  ear.  Those  sporadic  cases  which  have  been  followed 
by  eye  and  ear  lesions  are  probably  the  epidemic  form  and  due  to 
the  diplococcus  intracellularis. 

In  going  over  the  cases  of  meningitis  which  have  occurred  in  the 
City  Hospital  in  the  five  years  previous  to  the  appearance  of  the 
epidemic,  and  in  which  bacteriological  examinations  were  made 
at  the  post-mortem  examination,  no  cases  due  to  the  diplococcus 
intracellularis  were  found. 

This  matter  of  the  relation  of  sporadic  cases  to  the  epidemic 
form  is  one  of  the  greatest  importance,  and  can  only  be  deter- 
mined by  a  careful  bacteriological  examination  of  the  organs 
of  the  cases  which  die,  and  bacteriological  examination  of  the 
fluid  obtained  from  the  spinal  puncture  in  all  cases.  This  is  one 
gap  in  our  knowledge  of  the  disease  which  remains  to  be  filled  up. 
It  seems  probable  that  there  must  be  a  large  number  of  sporadic 
cases  of  epidemic  meningitis  constantly  occurring,  which,  under 
certain  conditions,  the  nature  of  which  we  are  not  aware  of,  may 
so  increase  in  number  as  to  form  an  epidemic.     Nothing  can  be 


30 

learned  with  regard  to  these  cases  from  an  examination  of  the 
mortality  tables.  One  gets  the  impression  from  such  tables  that 
the  disease  is  very  frequently  not  recognized  when  it  occurs,  and 
that  ma;ny  cases  are  reported  as  meningitis  which  are  not  so. 
The  large  percentage  of  cases  under  one  year  in  such  tables 
shows  how  unreliable  they  are. 


CLINICAL     CASES. 

The  description  of  individual  cases  is  taken  from  the  records  in 
the  three  hospitals  in  which  the  cases  occurred.  They  are  not 
reported  in  full,  but  the  most  important  of  the  phenomena  noted 
in  the  records  are  described.  These  records  have  been  made  by 
a  number  of  physicians,  and  they  represent  the  routine  hospital 
examinations  of  patients.  There  is  a  certain  advantage  in  having 
the  observations  of  a  number  of  men,  because  a  single  individual 
would  almost  certainly  have  his  attention  directed  to  single  clinical 
phenomena  which  seemed  to  him  of  special  importance  and  inter- 
est. The  cases  reported  by  Dr.  Williams^^^  are  included  in  this 
report.  A  number  of  charts,  which  are  illustrative  of  the  pulse 
and  temperature  of  the  disease,  is  given  with  the  individual 
cases. 

In  estimating  the  duration  of  disease,  the  time  of  onset  as  given 
in  the  history  of  the  patient  before  entry  into  the  hospital  is  taken. 
Many  of  the  patients  were  brought  into  the  hospital  in  an  uncon- 
scious condition,  and  were  without  relatives  or  friends  from  whom 
their  previous  history  could  be  obtained.  Many  of  them  were 
foreigners,  and  many  belonged  to  a  class  in  which  there  would  be 
but  little  attention  paid  to  the  early  symptoms  of  the  disease.  The 
charts  which  are  given  were  taken  after  the  patients  had  entered 
the  hospital,  and  after  the  disease  had  existed  a  variable  length  of 
time.  It  is  greatly  to  be  regretted  that  we  could  obtain  no  chart 
which  represented  the  entire  duration  of  the  disease,  nor  could  we 
find  any  such  in  the  literature. 

Case  1.  Female,  age  fifty  years.  Entered  hospital  June  21,  1896. 
Present  illness  began  three  days  before  admission.     At  that  time  frontal 


31 

headache,  constant  vomiting,  pain  in  small  of  back  and  both  calves.  On 
admission,  puj^ils  regular ;  some  general  tenderness  in  muscles  of  calves 
and  thighs ;  great  rigidity  of  neck ;  Avhole  body  can  be  raised  without 
bending  neck ;  movement  of  head  from  side  to  side  painful.  June 
22,  pujiils  contracted ;  great  pain  in  lumber  region ;  very  restless. 
Blood  count  showed  15,000  leucocytes.  June  23,  noisy  and  delirious. 
June  24,  delirium  continued.  June  25,  dysphagia ;  pupils  react  alike ; 
patient  cannot  be  roused.  Died  4.52  P.M  The  chart  shows  slight 
irregular  fever,  with  terminal  rise.     Post-mortem  examination. 


Case  2.  Female,  age  fourteen  years.  Entered  hospital  October  6, 
1896.  September  21,  complained  of  headache  and  pain  in  abdomen. 
After  one  week,  continual  nausea  and  vomiting,  followed  by  complete 
annorexia.  At  the  beginning  of  the  illness,  had  a  severe  chill.  On 
admission,  complained  of  pain  in  head,  neck,  and  generally  over  body  ; 
said  it  pained  her  to  move ;  pupils  equal ;  tenderness  on  pressure  over 
cervical  and  upper  dorsal  vertebrae  ;  attempts  to  flex  or  move  head  from 
side  to  side  causes  pain.  October  10,  patient  has  moaned  and  cried 
almost  continually  since  admission.  When  spoken  to,  complains  of 
pain.  From  this  time  until  death,  on  October  17,  the  condition  remained 
about  the  same,  the  patient  becoming  gi-adually  weaker.  The  chart 
shows  slight  increase  in  temperature,  with  great  irregularity.  Post- 
mortem examination. 


Case  3.  Male,  age  twenty-six  years.  Entered  hospital  Dec.  31,  1896. 
He  had  not  been  feeling  well  for  three  weeks  ;  was  found  unconscious 
on  bath-room  floor  (no  date  given),  and  was  still  unconscious  when 
brought  into  the  hospital.  UiDon  admission,  eyes  showed  slight  diverg- 
ent strabismus ;  pupils  much  contracted-,  equal,  do  not  react ;  slight 
retraction  and  rigidity  of  neck,  slight  rotation  to  left;  reflexes  increased. 
January  2,  patient  had  two  or  three  convulsions ;  extremities  rigid ; 
still  unconscious  ;  very  restless  ;  retraction  of  neck  increased.  January 
3,  condition  worse ;  still  unconscious.  January  4,  has  had  convulsions 
nearly  all  day,  with  short  intermissions ;  twitching  of  hands  and  face. 
January  4,  died. 


Case  4.  Male,  age  twenty-three  years.  Entered  hospital  Dec.  30, 
1896.  Three  days  before,  had  a  chill,  Avent  to  bed,  and  soon  began  to 
have  severe  headache  and  vomiting.  Two  days  previous,  had  been 
taking  care  of  a  child  which  died  of  "  inflammation  of  the  brain." 
Upon  admission,  very  restless,  complained  of  severe  pain  in  head  and 
neck;  eyes  normal.  December  31,  blood  count  showed  16,500  whites. 
January  6,  temperature  higher ;  epistaxis ;  delirious  for  past  two 
days.  January  11,  much  improved.  January  15,  improving  slowly. 
January  23,  temperature  normal.  January  26,  discharged  well.  The 
appended  chart  shows  the  highest  temperature  found  in  any  case  in  the 


32 


series,  with  the  exception  of  some  terminal  tempei-atiires. 
parison  of  the  pulse  with  the  temperature  is  interesting. 


The  com- 


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Case  5.*  Male,  age  forty  years.  Entered  hospital  January  2.  Dec. 
27,  1896,  went  to  work  as  usual,  when  severe  headache  came  on  ;  next 
day  delirious,  and  knew  no  one.  On  admission,  he  was  in  a  semi-coma- 
tose condition,  and  remained  so  until  death,  January  5.  Post-mortem 
examination. 


Case  6.  Female,  age  seven  years.  Entered  hospital  February  11. 
Three  weeks  before  admission,  violent  headache  and  vomiting  Four 
days  after  this,  became  deaf,  and  had  pain  in  both  ears.  No  discharge 
from  ears ;  has  had  marked  opisthotonos.  On  admission,  head  retracted 
and  drawn  to  right  side ;  eyes  bulging  ;  perfectly  deaf ;  complains  much 
of  pain.  February  13,  examination  of  ear  shows  otitis  media  on  right 
side ;  left  ear  shows  an  old  otitis  media.     Child  sent  to  surgical  wards 


*  The  following  cases  in  the  series  are  In  1897. 


33 

for  operation.  Re-entered  April  3,  after  mastoid  operation,  wound 
healed.  Child  very  much  emaciated ;  abdomen  retracted  ;  no  retraction 
of  head  ;  understands  very  little  ;  seems  to  have  no  perception  of  light ; 
hears  but  little,  if  any.  On  May  20,  can  recognize  light  and  shade. 
May  30,  much  stronger.  June  6,  can  stand  alone.  Can  see  contour  and 
light  and  shade.  June  10,  hearing  somewhat  improved ;  sees  somewhat 
better.  June  20,  discharged.  This  case  is  evidently  one  of  the  very 
chronic  forms  of  cerebro-spinal  meningitis.  Three  lumbar  punctures 
were  made,  the  turbidity  of  the  fluid  withdrawn  diminishing  in  the  suc- 
cessive punctures.  No  organisms  obtained ;  first  spinal  puncture  made 
four  weeks  after  onset 

Case  7.  Male,  age  forty  years.  Entered  hospital  February  10. 
For  a  week  before  entrance,  intense  nausea,  severe  pain  in  back  and 
legs.  A  day  after  onset,  was  unconscious,  and  moved  hands  and  feet 
convulsively.  Became  conscious  again  three  days  later,  and  talked 
rationally,  but  still  had  intense  pain  in  head,  back  and  legs.  From  the 
onset  there  was  frequent  vomiting.  On  admission,  somewhat  delirious  ; 
head  retracted ;  pupils  react  slightly  to  light ;  patellar  reflex  normal ; 
marked  tenderness  of  back  of  neck,  head  and  along  sjDinous  processes. 
February  15,  much  worse.  For  a  day  or  two  after  admission  was  de- 
lirious, but  now  is  semi-conscious.  There  is  paralysis  of  the  right  side. 
Passes  urine  involuntarily.  February  17,  temperature  high  ;  oedema  of 
lungs ;  unconscious,  cyanotic :  head  retracted  and  turned  to  right ;  no 
strabismus.    Died  at  4  p.m.     Post-mortem  examination. 

Case  8.  Male,  age  forty-nine  years.  Entered  hospital  February  7. 
Was  found  in  his  room  unconscious,  and  brought  to  the  hospital. 
Pupils  contracted,  and  do  not  react;  patellar  reflex  absent;  stiff- 
ness of  muscles  of  neck ;  pulse  of  good  strength  and  volume.  Patient 
remained  unconscious,  breathing  heavily  during  the  day,  and  towards 
night  moaned  and  had  convulsive  movements  of  ai'ms.  Lungs  began 
to  fill  up  in  the  afternoon.  Died  at  1.30  a.m.,  February  11.  Post-mortem 
examination. 

Case  9.  Male,  age  twenty -five  years.  Entered  hospital  February  12, 
with  a  diagnosis  of  acute  articular  rheumatism  and  unresolved  pneu- 
monia. About  that  tim,e  had  headache,  pains  and  swellings  in  hands 
and  knees.  Physical  examination ;  septic  odor  to  nasal  discharge ; 
throat  injected ;  pupils  dilated ;  mai'ked  tremor  of  hands  and  slight 
twitching  of  muscles ;  seems  dull,  somnolent,  but  when  roused  answers 
questions ;  reflexes  present.  February  16,  condition  about  the  same  as 
at  entrance.  February  20,  condition  much  improved.  Pain  and  swell- 
ing in  joints  much  better.  March  1,  examination  shows  flatness  under 
right  scapula  and  a  few  sub-crepitant  rales.  March  6,  dullness  in  right 
back  not  so  marked.  March  16,  condition  same  as  at  last  note.  Blood 
count  shows  20,000  w^hites.  March  21,  growing  gradually  weaker; 
dyspnoea  came  on  in  evening,  for  which  no  cause  could  be  found.  Died 
at  12.45  A.M. 


34 


Case  10.  Male,  age  ten  years.  Entered  hospital  February  23.  Four 
days  before  admission,  headache,  pain  in  stomach,  restlessness,  vomit- 
ing, and  constipation.  On  admission,  delirious  and  unmanageable  ;  head 
retracted ;  muscles  of  neck  tense  and  contracted ;  quite  deaf  since  en- 
trance. There  Tvas  very  little  increase  of  temperature  throughout  the 
disease;  eyes  normal.  Lumbar  puncture,  March  22,  thirty-one  days 
after  admission  and  thirty-five  days  from  beginning  of  disease,  showed 
slightly  clouded  fluid ;  no  organisms  found.  There  was  great  emacia- 
tion.    Child  discharged  relieved,  though  x^erfectly  deaf,  April  -4. 

Case  11.  Male,  age  thirty-one  years.  Entered  hospital  March  5. 
Has  been  having  severe  chills  for  two  weeks.  One  week  before 
entrance,  went  to  bed  complaining  of  pains   in  back  and   neck   and 


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headache.  Upon  admission,  slight  ptosis  of  right  lid ;  right  jnipil 
larger  than  left,  both  react ;  tenderness  behind  mastoids ;  pain  upon 
movement  of  head ;    lumbar  muscles   tender.     March  7,  blood  count 


35 


shows  19,000  whites.  March  9,  has  severe  headache  and  pain  in  back 
of  heck.  March  12,  pain  not  so  severe;  lumbar  puncture  negative. 
March  15,  nervous,  but  better.  March  27,  patient  up  and  doing  well. 
April  10,  discharged  well. 

Case  12.  Male,  age  twenty-one  years.  Entered  hospital  Mai-ch  4. 
Gave  up  work  two  weeks  before  admission.  Complained  of  head- 
ache, pain  in  neck,  loss  of  appetite.  The  headache  was  mainly  in 
the  occipital  region,  and  extended  into  upper  cervical  region  and 
both  eyes.  It  increased  in  sevei'ity  up  to  time  of  admission.  On  ad- 
mission, eyes  normal ;    head  held  stiffly  and  slightly  retracted ;    legs 


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weak ;  pulse  dicrotic.  March  8,  noisy  delirium.  Movement  of  head 
more  free.  OiDhthalmoscopic  examination  showed  slight  optic  neuritis. 
March  10,  lumbar  ijuncture,  patient  slept  quietly  after  it.  Stiffness 
of  neck  and  back  very  marked.  March  19,  rigidity  still  marked; 
patient  occasionally  cries  out.  March  19,  still  delirious,  but  more 
rational   than  before.     March  23,  ap^jarently  has   less  pain ;    answers 


36 


questions  intelligently.  On  the  27th,  decidedly  better,  no  pain,  head 
moved  freely.  From  this  time  the  patient  steadily  improved,  and  was 
dischai-ged  April  10.  The  fluid  from  spinal  puncture  made  March  10 
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Bee  Case  14. 


aj^parently  no  growth  after  twenty-four  hours,  but  after  this  there  was 
an  abundant  growth  of  typical  diplococci  just  above  the  water  of  con- 
densation. The  appended  chart  shows  a  rather  high  and  irregular 
temperature,  with  dro23  to  sub-normal  at  the  last.  The  pulse  is  low 
throughout. 


37 

Case  13.  Female,  age  three  years.  Entered  hospital  April  19.  On 
February  22,  acute  attack ;  convulsions,  vomiting,  high  fever ;  right 
eye  sw^ollen,  but  aftervi^ards  became  sunken.  On  admission,  retraction 
of  head.  Choroiditis  found  on  examination.  Lumbar  puncture,  April 
22,  gave  practically  clear  fluid ;  no  oi-ganisms  found.  Child  discharged 
unrelieved  April  29. 

Case  14.  Male,  age  seventeen  years.  Entered  hospital  March  6. 
Ten  days  before  admission,  pain  in  back  of  neck,  followed  by  a  chill 
and  extension  of  pain  to  head  and  back.  Three  days  before  admission, 
diplopia  and  deafness  in  left  ear.  Eight  days  before,  vomiting  and 
vertigo.  Had  been  in  bed  since  onset.  Was  more  or  less  delirious 
during  first  seven  days.  On  admission,  muscles  of  neck  tense ;  pupils 
equal  and  reacted ;  ptosis  of  left  eye,  and  photophobia.  March  10,  less 
pain  in  the  head.  March  12,  double  optic  neuritis.  Blood  count, 
March  11,  showed  16,000  leucocytes.  March  12,  left  ear  congested  over 
the  whole  extent  of  drum  March  14,  mild  delirium.  March  15,  blood 
count  showed  22,000  whites.  March  18,  condition  much  worse  ;  patient 
in  stupor,  which  continued  to  increase  until  March  21.  Death  at 
1.10  P.M.  Spinal  puncture,  March  15,  showed  8  cubic  centimeters  of 
clear,  watery  fluid.  No  sediment  Mici'oscopic  examination  showed  no 
cells.  Cultures  sterile.  March  18,  lumbar  puncture  gave  6  cubic  centi- 
meters of  a  slight  opalescent  wateiy  fluid,  with  trace  of  albumen.  No 
cellular  elements  No  organisms.  Cultures  sterile  after  forty-eight 
hours.  In  this  case  spinal  punctures,  made  nineteen  days,  twenty  days, 
and  twenty-two  daj^s  after  acute  onset,  were  negative,  both  for  organ- 
isms and  pus  cells.  The  temperature  in  this  case  is  interesting,  showing 
a  rapid  fall  to  normal  on  third  day  of  entrance,  after  which  there  were 
slight,  irregular  rises.     The  pulse  is  equally  irregular. 

Case  15.  Male,  age  fifteen  yeai's.  Entered  hospital  March  19. 
Three  weeks  before  admission,  complained  of  continuous  pain  in  head 
and  back.  For  three  days  before  admission  was  semi-conscious,  but 
responded  when  spoken  to.  Vomited  frequently.  On  admission,  semi- 
conscious ;  convergent  strabismus  of  right  eye  ;  some  diplopia;  pupils 
unequal,  and  did  not  react  alike ;  tache  cer6brale  well  marked ;  all 
reflexes  absent ;  no  tenderness  along  spine ;  at  times  mai'ked  retrac- 
tion of  head.  March  21,  purpuric  spots  observed  on  knees  and  flexure 
side  of  forearm ;  complete  unconsciousness ;  urine  and  fseces  passed 
involuntarily.  March  22,  patient  steadily  failed,  and  died  at  1.30  p.m. 
Lumbar  puncture  made  March  20  gave  6  cubic  centimetei'S  of  an  opal- 
escent watery  fluid,  which  deposited  slight  sediment.  Microscopic 
examination  showed  pus  cells  and  diplococci.     Cultures  positive. 

Case  16.  Male,  age  30  years.  Entered  hospital  March  18.  Twenty 
days  befoi'e  admission,  general  malaise  and  headache,  which  increased 
in  severity,  and  neck  became  stiff  and  rigid.  A  few  days  before 
entrance,  became  delirious.    On  entrance,  noisy  and  delirious.     At  times 


38 

violent  rigidity  of  muscles  of  neck ;  head  retracted ;  tenderness  along 
cervical  and  dorsal  region;  pupils  equal  and  i-eacted  alike;  eyeballs 
rolled  up ;  rigidity  of  muscles  of  extremities.  March  22,  continuous 
delirium  and  coma  a  few  hours  before  death.  Death,  4  p.m.  Lumbar 
puncture  on  March  22,  shortly  after  death,  gave  5  cubic  centimeters  of 
clear  straw-colored  fluid,  with  slight  flocculent  sediment.  On  micro- 
scopic examination,  numerous  lymphoid  cells ;  no  pus  cells ;  no  organ- 
isms ;  cultures  sterile.  In  this  case  the  lumbar  puncture  was  made 
twenty-four  days  after  acute  onset. 

Case  17.  Female,  age  twelve  years.  Entered  hospital  March  8. 
One  week  before  entrance,  headache ;  burning  feeling  in  head ;  pain 
about  eyes ;  vomiting ;  rather  stupid  three  days  before  entrance ;  stiff- 
ness of  neck.  On  admission,  marked  retraction  of  head,  with  stiffness  ; 
slight  convergent  strabismus ;  could  answer  questions  intelligently. 
Blood  count  showed  9,800  whites.  Herpes  of  lips;  large  patches  of 
herpes  on  left  arm;  few  hsemorrhagic  spots  on  abdomen.  March  11, 
brighter;  no  tenderness  along  spine.  Lumbar  puncture  negative 
Blood  count  gave  19,0U0  whites.  Eye  examination  showed  atrophy  of 
optic  nerve  on  left  side.  Another  blood  count  gave  22,000  whites.  On 
March  23,  blood  count  gave  26,000  whites.  Condition  changed  con- 
stantly ;  one  minute  would  complain  of  headache,  and  then  of  no  pain, 
April  1,  vomited.  April  2,  no  vomiting.  No  change.  April  5,  blood 
count  gave  20,000  whites.  April  8,  vomited  during  night.  April  9, 
vomiting  continued.  April  1 1 ,  headache  most  of  the  day.  April  13,  more 
comfortable.  April  16,  severe  headache  ;  retraction  of  head  diminished. 
April  23,  culture  from  nasal  mucous  membrane  negative.  April  26, 
temperature  practically  normal.  May  6,  still  complained  of  headache ; 
vomiting.  May  20,  much  better.  May  22,  pain  in  legs.  Blood  count 
showed  14,000  whites.  Patient  discharged  well  June  12,  Some  tendency 
to  walk  on  heels. 

Case  18.  Male,  age  eight  years.  Entered  hospital  March  5,  Three 
days  before  enti'ance,  headache,  pain  in  stomach,  vomiting.  On  ad- 
mission, tenderness  over  entire  body,  chiefly  in  neck ;  head  retracted. 
For  next  three  days  retraction  continued ;  muscles  tense.  Lumbar 
puncture  on  Mai-ch  9,  eight  days  after  acute  attack,  gaA^e  cloudy  fluid. 
April  3,  macular  eruption  noted  over  legs  and  trunk.  Continued  to  gain 
gradually.  Discharged  well  on  May  10,  1897.  In  this  case  lumbar 
puncture  was  performed  three  times  at  different  periods  of  the  disease. 
There  was  constant  diminution  in  the  turbidity  of  the  fluid :  1st,  very 
turbid,  with  thick  purulent  sediment ;  2d,  less  marked ;  3d,  slightly 
cloudy;  some  fibrin  formed  in  the  fluid,  but  there  was  no  purulent 
sediment.     Diplococci  uncertain. 

Case  19,  Male,  age  twenty-two  years.  Entered  hospital  March  5. 
Day  before  admission,  pain,  slight  cough,  vomiting,  headache,  chill  in 
evening.     Tried  to  work  morning  of   admission,  but  became  drowsy 


39 

and  vomited  several  times.  Oa  admission,  conjunctivEe  injected ;  skin 
hyper^emic ;  reflexes  normal.  In  evening,  several  convulsive  attacks ; 
eyes  varied  ;  part  of  time  left  pupil  dilated,  at  other  times  equal ;  right 
eye  turned  in  at  times.  March  6,  worse ;  head  somewhat  retracted. 
Died  at  8.45  P.M.    Post-mortem  examination. 

Case  20.  Male,  age  five  years.  Entered  hospital  March  11.  One 
week  before  entry,  vomited  and  had  chilly  sensation ;  pain  in  stomach 
and  headache.  Herpes  on  admission ;  red  spots  on  abdomen  ;  held  head 
stiffly ;  no  retraction ;  pupils  equal ;  slight  tenderness  in  back  of  neck, 
none  along  lower  part  of  spine  or  mastoids  ;  irritable  ;  patellar  reflexes 
diminished.  Blood  showed  36,0U0  whites.  Eye  examination  showed 
indistinct  discs,  more  marked  in  right  eye.  Face  congested.  March  15, 
optic  discs  more  distinct  than  at  first  examination.  March  16,  neck  not 
so  stiff.  March  18,  blood  count  showed  24,000  whites.  March  22,  neck 
painful ;  stiffness  of  neck,  but  no  retraction.  Blood  count  showed 
22,000  whites.  Discharged  well  April  1.  Last  blood  count,  March  30, 
showed  8,100  whites. 

Case  21.  Male,  age  twenty-three  years.  Entered  hospital  March 
10.  Five  days  before,  complained  of  pain  in  head,  neck,  back  and  limbs  ; 
on  the  same  day  became  delirious.  Upon  admission,  eyes  normal ; 
physical  examination  negative  ;  mental  condition  seemed  dull ;  he  talked 
strangely.  March  14,  delirium  less  ;  resisted  treatment.  Lumbar  punct- 
ui'e,  milky  fluid  withdrawn.  March  18,  patient  got  out  of  bed  and 
wandered  about;  seemed  brighter.  March  26,  patient  remained  in  a 
condition  of  semi-stupor,  March  81,  vomited  yesterday,  and  seemed 
weaker.     April  4,  abdomen  "  scaphoidal."    Died  April  6. 

Case  22.  Male,  age  twenty-five.  Entered  hospital  March  9.  Twenty- 
four  hours  before  admission  he  complained  of  headache,  and  during  the 
evening  was  found  unconscious  on  the  floor  of  his  room.  On  admission 
into  hospital,  unconscious ;  muscles  of  back  and  neck  stiff'  and  rigid ; 
head  retracted ;  pupils  dilated ;  patellar  reflex  increased.  March  10, 
condition  the  same.  A  blood  count  showed  19,800  leucocytes.  On 
March  12,  patient  still  unconscious ;  became  comatose,  and  died  at 
11.15  a.m.  on  March  13,  The  temperature  was  100*^  at  time  of  admis- 
sion, and  showed  a  gradual  increase,  reaching  104°  on  the  last  day. 
Post-mortem  examination. 

Case  23.  Male,  age  23  years.  Entered  hospital  March  11.  Three 
days  before  admission,  complained  of  pain  in  back,  headache  and  ner- 
vousness ;  on  night  before  admission,  became  delirious  and  vomited  a 
great  deal.  On  admission,  was  very  restless;  no  retraction  of  head; 
pupils  equal,  and  reacted  alike  ;  patellar  reflex  absent ;  legs  held  rigidly. 
Patient  resisted  examination.  March  12,  patient  very  stupid ;  lay  on  left 
side ;  no  apparent  tenderness  over  ma.stoid  region.  March  13,  dark-red 
eruption  over  trunk  and  extremities ;  patient  rational ;  tongue  protruded 


40 

slightly  to  the  left.  March  15,  general  condition  better.  Mental  condi- 
tion improved ;  slight  convergent  strabismus  of  right  eye.  All  the 
sym^Dtoms  continued  to  improve,  and  he  was  discharged  well  April  13. 
Spinal  puncture,  made  March  20,  gave  8  cubic  centimeters  of  clear 
watery  fluid,  with  very  slight  floculent  sediment.  Microscopic  examina- 
tion showed  a  few  lymphoid  cells,  but  no  polynuclears.  No  organisms 
found  microscopically.  On  cultures  after  several  days  there  developed 
very  small  colonies  of  diplococci,  which  varied  considerably  in  size,  but 
which  showed  the  characteristic  staining. 

Case  24.  Female,  age  five  years.  Entered  hospital  March  18. 
Ten  days  before  admission,  poor  appetite  on  returning  from  school ; 
next  day,  dull,  cried  much  ;  kept  eyes  closed  most  of  the  time ;  screamed 
once  or  twice,  as  if  in  severe  pain  ;  herpes  of  lips.  Retraction  of  head 
and  inequality  of  pupils  noticed  on  day  of  entry.  The  mother  said  that 
another  child  in  her  neighborhood  had  similar  symptoms,  and  died  in 
eight  days.  On  admission,  head  retracted;  eyes  closed;  pupils  large 
and  equal,  and  changed  from  time  to  time ;  reacted  sluggishly  to  light ; 
slight  convergent  strabismus  ;  no  tenderness  of  mastoids  or  along  spine ; 
purulent  secretion  on  conjunctiva.  Blood  count  showed  18,000  whites. 
March  21,  no  change  in  condition;  spoke  occasionally  to  nurse;  eyes 
closed  most  of  the  time.  March  26,  evidence  of  broncho-pneumonia. 
March  30,  blood  count  showed  16,000  whites.  April  2,  no  particular 
change ;  left  chest  still  dull ;  retraction  of  head  the  same.  April  5, 
blood  count  showed  21,000  whites.  April  8,  left  lung  cleared  up.  April 
13,  fretful ;  retraction  continued.  April  14,  discharge  from  right  ear. 
April  16,  both  ears  discharging.  April  19,  discharge  from  ears  much 
less.  April  21,  retraction  of  head  extreme;  eye  symptoms  the  same. 
April  28,  ear  discharge  slight.  April  30,  ear  discharge  profuse.  May 
9,  severe  cough,  with  rapid  respiration.  May  10,  collapse  during  morn- 
ing; continued  to  grow  weaker,  and  died  at  10.30  a.m.  of  the  12th. 
April  23,  cover-slips  from  nose  and  from  ear  discharge  showed  dip- 
lococci decolorized  by  Gram  in  the  leucocytes.  No  diplococci  found  in 
the  sputum  examined  May  9.  The  temperature  chart  of  the  case  is 
interesting,  as  showing  a  continuous  high  temperature,  running  above 
103^. 

Case  25.  Female,  age  seventeen  years.  Entered  hospital  March  11. 
March  9,  had  chill,  headache,  pain  all  over  body,  pain  in  eyes,  and  throb- 
bing in  ears  which  interfered  with  hearing ;  vomited  several  times.  On 
admission,  slight  nystagmus ;  pupils  equal  and  reacted  alike ;  reflexes 
normal ;  tache  cerebrale  well  marked.  March  12,  intense  pain  in  back 
and  neck.  March  13,  vomited  several  times  ;  slight  delirium ;  dijilopia, 
convergent  strabismus  and  slight  ptosis ;  tenderness  on  pressure  along 
spine.  Blood  count  showed  31,000  white  corpuscles  on  Mai'ch  14.  Deli- 
rium continued ;  could  be  roused  to  answer  questions.  March  16,  patient 
much  duller,  and  died  at  3.30  p.m.  Spinal  puncture,  March  14,  gave  8| 
cubic  centimeters  of  cloudy  fluid,  with  slight  sediment.     On  microscopic 


41 

examination,  abundant  pus  cells  were  found  containing  numbers  of 
diplococci.  Cultures  showed  abundant  pure  growth  of  diplococci.  The 
chart  shows  a  rise  to  105|°  the  second  day  after  entering  hospital,  then 
a  fall  to  normal,  followed  by  a  rise  to  1U2"  at  death. 

Case  26.  Female,  age  25  years.  Entered  hospital  March  17.  Sick 
four  days  before  entrance ;  com^Dlained  of  headache  and  of  indefi- 
nite pain  all  over  body ;  this  was  followed  by  delirium  and  vomiting. 
On  admission,  pupils  regular  and  reacted ;  reflexes  normal.  March  20, 
slight  nystagmus  and  diplopia ;  marked  tenderness  in  back  of  neck. 
March  25,  sixth  nerve  paralyzed  on  right  and  partially  on  left  side ; 
constant  variable  nystagmus  ;  answered  questions  slowly ;  was  lethargic. 
March  26,  paresis  of  third  nerve  ;  optic  nerves  showed  slight  swelling  and 
congestion.  March  30,  vomiting ;  patient  much  weaker ;  stupor  appear- 
ing. April  2,  stupor  increased,  and  patient  died  at  5.55  A.  M.,  April  3. 
Lumbar  puncture,  April  3,  shortly  after  death,  gave  a  small  amount  of 
turbid  fluid.  No  microscopic  examination  made  of  the  fluid.  It  was 
sterile  in  cultures. 

Case  27.  Female,  age  two  and  one-half  years.  Entered  hospital 
April  8.  Sickness  began  twenty-five  days  before  entry  into  hospital 
with  headache,  loss  of  vision  and  vomiting.  On  admission,  emaciated ; 
head  not  retracted,  but  some  resistance  to  flexion,  April  11,  lumbar 
puncture  gave  turbid  fluid  with  slight  deposit  of  pus  at  bottom  of  tube  ; 
diplococci  in  pus  cells.  Chart  shows  irregular  sharp  rise  in  tempera- 
ture up  to  106"  before  death. 

Case  28.  Male,  age  thirty-seven  years.  Entered  hospital  March  20. 
One  week  before  admission,  headache,  pain  and  stifl'ness  in  neck ; 
three  days  before  admission,  was  delirious.  On  admission,  head  rigid, 
patient  cried  out  with  pain  on  attempting  to  move  it ;  delirium ;  head 
retracted ;  jjupils  contracted,  but  reacted  alike ;  patellar  reflex  absent. 
March  24,  continued  delirium ;  back  and  neck  painful  to  touch.  Blood 
count  gave  l'i,000  whites.  On  March  28,  quieter  and  more  rational. 
April  1,  less  tenderness  and  rigidity;  no  special  change  of  mental  condi- 
tion ;  no  optic  neuritis.  April  5,  still  delirious  and  restless,  April  9, 
some  improvement ;  the  mind  clear  at  times.  April  13,  continuous  im- 
provement. April  17,  mental  condition  better,  but  at  times  delirious. 
The  patient  continued  to  gain  in  strength,  and  on  May  17  was  dis- 
charged, to  go  into  country.  At  the  time  of  discharge,  irritable  and 
childish.  Lumbar  puncture,  March  24,  was  negative  for  organisms  both 
on  microscopic  examination  and  cultures.  There  were  abundant  pus 
cells  in  the  fluid. 

Case  29.  Female,  age  four  and  one-half  years.  Entered  hospital 
March  20.  Attack  began  three  days  before  entrance ;  vomiting ; 
after  that  great  pain  in  head  and  neck  ;  opisthotonos.  Lumbar  puncture 
made  March  20.    Optic  neuritis  of  both  sides  on  May  15.     Child  con- 


42 

tinued  to  improve,  and  was  discharged  well  June  6.  Temperature  of 
the  case  is  interesting,  as  showing  a  very  low  temperature,  rising  only 
•once  to  101°.  Fluid  from  lumbar  puncture,  March  20,  was  cloudy  but 
not  very  turbid  ;  only  slight  deposit. 

Case  30.  Female,  age  three  years.  Entered  hospital  March  24. 
Four  days  before  admission,  tenderness  of  neck  muscles  ;  hyperesthesia 
of  entire  body,  Lumbar  jjuncture  positive.  Herpes  of  lips.  Condition 
improved  rapidly,  temperature  falling  to  normal  on  March  28.  Dis- 
charged well  April  12. 

Case  31.  Female,  age  eight  years.  Entered  hospital  March  23. 
Three  days  before  admission,  vomiting,  pain  in  back,  headache  and 
constipation.  Strabismus  two  days  before  admission.  .On  admission, 
strabismus  of  both  eyes ;  hyperesthesia  of  entire  body,  chiefly  back 
of  neck  ;  patellar  reflexes  normal.  Lumbar  puncture,  March  26,  nega- 
tive. At  this  time,  temperature  was  gradually  going  down.  Lumbar 
I^uncture,  April  3,  positive.  Discharged  well  July  5.  The  spinal  punct- 
ure was  made  during  an  exacerbation  of  fever. 

Case  32.  Female,  age  seventeen  years.  Entered  hospital  March  2.5. 
]March  21,  came  home  from  work  complaining  of  pain  in  head, 
chilliness  and  vomiting.  On  the  following  morning,  rigidity  of  arms 
and  legs,  with  slow  movements ;  was  in  stupor  and  unconscious  for 
most  of  the  day.  On  third  and  fourth  days,  delirious,  and  complained 
of  pain  in  head  and  neck.  On  admission,  muttering  delirium  ;  marked 
retraction  of  head ;  pupils  equal  and  reacted  to  light ;  convergent  strabis- 
mus. Patient  died  suddenly  at  6,30  a.m.,  March  26.  Temperature  on 
admission,  100^  ;  pulse,  120.     Post-mortem  examination. 

Case  33.  ]\Iale,  age  twenty- five  years.  Entered  hosj)ital  March  30. 
Eight  days  before  admission,  feeling  of  malaise,  with  headache.  Two 
daj's  before  entrance,  delirious ;  in  the  evening  was  nauseated.  On 
admission,  semi-conscious ;  fever  and  headache,  pain  in  neck ;  herpes 
on  lips  and  nose;  puj^ils  equal,  occasionally  strabismus  of  left  eye; 
knee  jerk  not  obtained.  April  2,  patient  unconscious.  Blood  count 
showed  21,600  whites.  Became  gradually  weaker,  and  died  at  10  p.m. 
Spinal  puncture,  made  April  2,  gave  temporary  relief.  Puncture 
showed  considerable  cloudy  fluid.  Smears  showed  abundant  pus  and 
dijDlococci. 

Case  34.  Female,  age  seven  years,  two  months.  Entered  hospital 
March  26.  Two  days  before  admission,  face  flushed,  complained  of 
headache,  vomiting.  There  were  convergent  strabismus  and  opisthot- 
onos. On  admission,  child  crying,  with  eyes  partly  closed  and  hands  to 
head.  Easily  roused  ;  answered  questions.  Pain  in  forehead ;  jjupils  re- 
acted alike  ;  convergent  strabismus  ;  tenderness  of  neck  ;  tache  cerebrals 
well  marked ;    patellar  reflexes  unequal.    Blood  count  showed  25,000 


43 

whites.  March  27,  restless  ;  tenderness  of  right  wrist,  which  was  swollen 
and  red ;  moderate  retraction  of  head ;  internal  strabismus ;  stupor ; 
complained  of  tenderness  of  right  ankle.  March  28,  vomiting  ceased ; 
stupor  increased.  March  29,  large  patch  of  hei-pes  just  below  and 
anterior  to  lobe  of  left  ear.  Culture  from  fluid  from  hei'petic  vesicles 
negative.  April  15,  much  better.  Discharged  well  May  4.  Tempera- 
ture was  high  until  April  2,  then  gradually  declined. 

Case  35.  Male,  age  five  years.  Entered  hospital  April  3.  Nine 
days  before  admission,  headache ;  irritable.  Two  days  before,  went 
to  Eye  and  Ear  Infirmary  and  was  sent  to  hospital.  On  entrance, 
right  pupil  slightly  larger  than  left ;  no  herpes  ;  no  ecchymosis  ;  slight 
stifi"ness  of  neck.  April  4,  much  pain  in  head  and  neck;  at  6  p.m., 
delirious;  quieter  afterwards.  April  5,  less  delirious.  April  7,  left  pupil 
larger  than  right ;  strabismus ;  slight  stiftness  of  neck ;  backward  and 
forward  movement  caused  jjain.  April  8,  did  not  recognize  relatives ; 
seemed  more  stupid ;  no  strabismus.     Discharged  against  advice. 

Case  36.  Male,  age  nineteen  years.  Entered  hospital  March  30. 
Five  days  before  admission,  pain  in  side,  severe  headache ;  vomiting, 
with  delirium  and  retraction  of  head.  On  admission,  delirious  and  deaf ; 
herpes  labialis  ;  pupils  equal  and  reacted  alike  ;  patellar  reflex  slightly 
increased.  Blood  count  showed  9,350  whites.  April  3,  retraction  less 
marked;  had  grown  more  deaf.  April  6,  head  moved  without  pain- 
April  12,  better.  Ophthalmoscopic  examination,  April  16,  showed  slight 
optic  neuritis.     April  19,  discharged. 

Case  37.  Male,  age  twelve  years.  Entered  hospital  April  1.  Vomit- 
ing and  headache  three  days  before  entrance.  On  entrance,  photophobia ; 
hyperjBthesia  of  skin,  no  eruption ;  delirious,  unconscious.  Herpes  de- 
veloped, general  condition  became  much  woi'se.  Died  April  7.  No 
post-mortem  examination.  Purulent  discharge  from  eyes.  Tempera- 
ture irregular,  with  sharp  terminal  rise.  Lumbar  puncture,  immedi- 
ately after  death,  gave  thick  purulent  fluid  with  diplococei  in  pus  cells 

Case  38.  Male,  age  thirty -thi-ee  years.  Entered  hospital  April  1. 
Three  days  before  admission,  began  to  vomit,  and  continued  to  do 
so  since;  pain  in  back  of  head.  On  admission,  pupils  equal,  slight 
convergent  strabismus  of  left  eye;  patellar  reflex  absent;  stiffness 
of  neck ;  pain  limiting  motion  in  all  directions ;  no  tenderness ;  no 
retraction.  April  4,  very  delirious,  tearing  his  bed.  April  5,  rapid 
failure ;    death  in  coma,  3  p.m. 

Case   39.    Male,  age  thirteen  months.    Entered  hospital  April   13. 

Two  weeks  before  admission  grew  feverish ;  loss  of  appetite ;  cried  a 

great  deal.    Four  days  before  admission,  slight  convulsion.     Head  re- 

'  tracted  five  days  before  admission.     Eyes  reacted  alike  ;  tache  cerebrale 

on  admission;  skin  clear.     Grew  gradually  worse;  died  May  18. 


44 


Case  40,  Male,  age  three  and  one-half  years.  Four  days  before 
admission,  fever  and  chills;  vomiting  day  before  admission;  head  re- 
tracted; slight  discharge  from  both  ears.  Lumbar  puncture,  April  8; 
fluid  very  turbid,  with  thick  pus  at  the  bottom  of  test  tube ;  diplococci. 
Died  June  14.    Post-mortem  examination. 

Case  41.  Female,  age  fifteen  years.  Entered  hospital  April  3.  On 
April  2  she  was  irritable,  had  intense  headache  and  vomiting.  On  day 
of  admission,  was  delirious  and  had  marked  muscular  spasm.  No 
retraction  of  head,  although  flexion  was  resisted,  and  there  was  con- 
siderable pain  and  tenderness  in  back  of  neck.  At  times  divergent 
strabismus  and  slight  nystagmus.  Pupils  dilated,  of  equal  size  and 
reacted  alike.  April  4,  the  same  condition  ;  frequent  vomiting  and  com- 
plained of  headache.    Died  suddenly.     Post-mortem  examination. 

Case  42  Male,  age  nineteen  years.  Entered  hospital  April  3.  Well 
up  to  night  before  admission.  Sickness  began  with  chill,  followed  by 
nausea  and  vomiting.  He  became  stupid  and  somewhat 
delirious.  On  admission,  pupils  somewhat  dilated, 
reacted  to  light ;  jaws  closed ;  no  retraction  of  head ; 
knee  jerks  noi-mal.  April  4,  delii'ious ;  in  semi-lucid 
intervals  complained  of  head ;  tenderness  of  muscles 
in  back  of  neck.  April  5,  breathing  somewhat  labored. 
Blood  count  showed  18,000  whites.  Died  at  3  p.m. 
Post-mortem  examination. 


EL 


Case  43.  Male,  age  thirty  five  years.  Entered  hos- 
pital April  5.  Two  days  before  admission  complained 
of  headache  and  intense  pain  through  head ;  jDain  also 
in  back  and  limbs.  The  day  before  admission,  became 
delirious  and  later  unconscious.  On  admission,  vmcon- 
scious,  pulse  full ;  neck  retracted ;  pupils  slightly 
conti'aeted,  reacted  alike ;  extremities  rigid ;  pain  on 
pressure  along  back  of  neck  and  spine.  April  6, 
very  cyanotic.  The  removal  of  exudation  by  lumbar 
puncture  was  followed  by  relief,  but  the  patient  soon 
grew  worse,  and  died  at  6.20  pm.  About  5  cubic 
centimeters  of  distinctly  cloudy,  purulent  fluid  was 
obtained  from  lumbar  puncture.  Smears  showed  pure 
pus,  many  of  the  pus  cells  very  large  and  filled  with 
flattened  diplococci. 


Case  44.  Male,  age  fifty  years.  Entered  hospital 
April  4.  No  previous  history  could  be  obtained.  On 
admission,  the  head  was  drawn  down  to  the  right 
posteriorly,  rotation  to  the  left  caused  intense  pain ; 
marked  tenderness  on  pressure  below  mastoids  ;  pupils  equal  and  reacted 
alike  ;  nystagmus  jiresent ;  patellar  reflex  absent.  Patient  failed  rapidly, 
and  died  April  9.     Post-mortem  examination. 


45 

Case  45.  Female,  age  four  and  one-half  years.  Entered  hospital 
April  9.  Sudden  attack  day  before  entrance,  with  headache,  etc., 
then  became  unconscious,  delirious  and  stupid.  Marked  hyperesthesia; 
tonic  spasms  of  arms  and  legs  Lumbar  puncture,  April  22,  showed 
cloudy  fluid,  with  jdus  cells  and  diplococci.  Child  continued  to  grow 
worse.     Died  May  24. 


Case  46.  Female,  age  eight  years.  Entered  hospital  April  9. 
On  admission,  unconscious ;  head  retracted.  Condition  became  worse, 
and  child  died  April  11.  Lumbar  puncture,  April  11,  showed  very  thick 
purulent  fluid,  with  pus  cells  and  diplococci.     Post-mortem  examination. 


Case  47.  Female,  age  twenty  years.  Entered  hospital  April  14. 
Headache  and  constant  vomiting  four  days  before  admission,  then 
became  unconscious  and  delirious.  Cried  out  with  pain  in  her  head, 
which  was  slightly  retracted;  muscles  of  neck  tense;  eyes  partially 
closed;  slight  divergent  strabismus  ;  both  pupils  somewhat  contracted  ; 
herpes  about  lips ;  patellar  reflex  normal ;  tache  cerebrale  marked. 
April  15,  vomiting  continued ;  rather  brighter ;  answered  questions  intel- 
ligently. April  17,  more  stupid;  delirious.  Blood  count,  April  18, 
showed  13,000  whites.  April  21,  slept  well;  no  vomiting;  less  rigid. 
Blood  count  showed  20,000  whites.  April  23,  vomiting  during  night. 
Patient  continued  to  improve  slowly,  and  was  discharged  relieved 
June  23.  Covei'-slip  examination  of  nasal  secretion  showed  diplococci 
decolorized  by  Gram  in  leucocytes  and  free. 


Case  48.  Female,  age  six  years.  Entered  hospital  April  19. 
Eight  days  before  admission,  fever  and  vomiting ;  severe  headache ; 
retraction  of  head  the  night  before  admission,  with  frequent  vomiting. 
After  admission,  had  slight  convulsion  and  became  unconscious  ;  after- 
wards hyperassthetic,  and  then  unconscious  again.  Died  shortly  after- 
wards, on  day  of  admission.  Lumbar  puncture,  after  death,  gave  slightly 
cloudy  fluid  ;  no  organisms  found. 


Case  49.  Male,  age  thirty-five  years.  Entered  hospital  April  22. 
Ten  days  before  admission,  comj^lained  of  headache  and  vomiting ; 
vomiting  persisted  for  several  days.  On  admission,  patient  in  stupor ; 
answered  no  questions  ;  muscles  of  back  of  neck  not  tense  except  when 
head  was  bent  forward  ;  abdomen  retracted.  Blood  count  showed  14,000 
whites.  April  23,  rigidity  of  back  of  neck  quite  marked.  April  25,  bed 
sore  developed.  Died  April  26,  Fluid  from  spinal  puncture,  made 
April  24,  was  slightly  cloudy.  Direct  examination  for  bacteria  negative. 
Polynuclear  leucocytes  present  in  moderate  numbers.  Cultures  on  two 
tubes  sterile ;  in  one,  colonies  of  staphylococcus  albus,  evidently  skin 
contamination.     The  temperature  shows  a  rapid  terminal  rise  to  107 -. 


46 


Case  50.  Female,  age  tliirty-six  years.  Entered  hospital  April  22. 
On  April  12,  had  chill;  headache  and  pain  running  down  the  ba^'k 
into  the  extremities.  Vomited  up  to  four  days  before  admission ;  was 
delirious  the  day  before  admission.  On  admission,  herpes  labialis ; 
pupils   equal  and  reacted ;  reflexes  normal ;  stiffness  of  neck ;   motion 


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growth  of  the  diplococcus.  The  cultures  were  made  by  pouring  1  cubic 
centimeter  of  the  fluid  over  slanting  test  tubes  of  serum.    One  colony 


47 


developed  on  one  tube,  three  on  a  second  and  none  on  four  others 
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Case  50  Concluded. 

Case  51.  Male,  age  fifty  years.  Entered  hospital  April  13.  Patient 
found  in  a  vacant  building.  On  admission,  unable  to  talk  ;  pupils  small 
and  equal;  slight  fibrillar  twitchings  of  muscles;  partial  anassthesia. 
April  14,  patient  fairly  i-ational.  April  16,  optic  neuritis,  with  con- 
vergent strabismus.  April  20,  delirious  ;  herpes  on  face  ;  some  petechias 
on  buttocks ;  no  vomiting,  no  headache.  Steadily  failed,  and  died  9.25 
P.M.  Lumbar  puncture,  April  15,  gave  15  cubic  centimeters  of  slightly 
cloudy,  watery  fluid,  with  slight  sediment.  Microscopic  examination 
showed  pus  cells,  with  occasional  diplococci.  Cultures  showed  very 
feeble  growth  of  typical  diplococci. 

Case  62.  Male,  age  twenty-seven  years.  Entered  hospital  April  14. 
On  day  before  admission,  had  a  chill;  delirious;  face  cyanotic; 
tongue  dry ;  left  pupil  smaller  than  right,  both  reacted  alike ;  no  en- 


48 

largement  of  spleen ;  legs  covered  with  reddish  hypersemic  blotches ; 
similar  condition  on  arms,  but  less  marked;  patellar  reflex  normal. 
Condition  grew  rapidly  worse.  Died  at  7.15  p.m.  Temperature  on 
entrance,  105^.    Post-mortem  examination. 

Case  53.  Male,  age  twenty-four  years.  Entered  hospital  April  17. 
Headache  and  vomiting  three  days  before  admission.  Upon  ad- 
mission, stiffness  of  neck,  pain  on  bending  neck  forward ;  herpes 
labialis ;  pupils  equal  and  regular,  reacted  alike ;  reflexes  normal ; 
hgemorrhagic  peteehise  on  elbow  and  buttocks.  On  April  21,  patient 
was  delirious ;  required  restraint,  but  was  occasionally  brighter  and 
answered  questions  intelligently.  Gradually  became  worse,  and  died 
at  3.45  P.M.,  April  23.    Post-mortem  examination. 

Case  54.  Male,  age  twenty-six  years.  Entered  hospital  April  15, 
Three  days  before  admission,  severe  headache ;  excessive  vomiting ; 
jjain  in  back,  especially  in  right  lumbar  region.  No  reti'action  of  neck 
when  admitted  into  hospital ;  mai'ked  resistance  to  movement  of  head ; 
tenderness  over  mastoids  and  right  lumbar  muscles ;  slight  ptosis  of 
light  lid ;  pupils  reacted  slowly,  but  equally.  April  20,  condition  im- 
proved. Aj^ril  23,  complained  of  pain  in  right  wrist.  May  3,  marked 
nausea  and  vomiting.  May  7,  vomiting  and  intense  headache.  May  11, 
very  delirious.  iMay  13,  severe  frontal  headache.  May  14,  difi'use 
sweating,  weaker  pulse.  May  17,  nausea  and  vomiting  continued. 
Lumbar  puncture,  made  April  19,  showed  a  small  amount  of  clear 
serous  fluid :  cultures  of  this  sterile.  Condition  gradually  imj)roved, 
and  j)atient  discharged  May  15.  This  case  is  not  clear.  The  history  is 
strongly  suggestive  of  mening'itis,  but  the  clear  serous  fluid  withdrawn 
by  spinal  i^uncture  sj)eaks  against  it. 

Case  55.  Female,  age  forty  years.  Entered  hospital  May  6.  Head- 
ache three  weeks  before.  Head  held  somewhat  backwards.  Vomiting 
for  a  week.  Day  before  entrance,  fell  unconscious.  On  admission, 
pupils  reacted  ;  tenderness  of  back  of  neck  ;  very  slight  rigidity ;  knee 
jerks  diminished.  White  corpuscles,  19,000.  Continued  more  or  less 
unconscious.    Died  May  8. 

Case  56.  Female,  age  three  and  one-half  years.  Entered  hosj)ital 
April  19.  Hlness  began  four  days  before  admission,  with  incessant 
vomiting.  Three  days  before  admission,  stiffness  of  neck,  with  great 
pain  on  motion.  No  strabismus.  On  entry,  cyanotic ;  dulness  at 
base  of  both  lungs ;  no  retraction  of  head ;  no  especial  tenderness 
along  spine.  One  hour  after  admission,  pupils  contracted ;  cyanosis 
worse.  Gradual  improvement  up  to  6  p.m.,  when  the  respiration  be- 
came diflBcult ;  unconsciousness  developed.  Died  on  morning  of  20th. 
Post-mortem  examination. 

Case  57.  Male,  age  twenty-four  years.  Entered  hospital  April  17. 
Perfectly  well  up  to  day  before  admission,  when  he  awoke  with  intense 


49 


headache,  vomited  several  times,  was  very  restless.  On  admission, 
almost  complete  unconsciousness,  turning  from  side  to  side,  burying  his 
head  in  the  pillow.  No  retraction  of  head  and  no  tenderness  at  back  of 
neck.  The  pupils  were  normal.  Patient  continued  very  restless,  turning 
from  side  to  side  :  restraint  was  necessary.  He  suddenly  showed  signs 
of  failure,  cyanosis,  weak  pulse,  and  died  at  4  15  p.m.,  three  hours  after 
admission.    Post-mortem  examination. 

Case  68.  Male,  age  twenty-eight  years.  Entered  hospital  April 
23.  One  week  before  admission,  complained  of  headache,  which 
was  followed  by  delirium  two  days  later.  On  admission,  high 
delirium,  patient  struggling  violently ;  rigidity  of  muscles  of  neck ; 
opisthotonos ;    pupils  dilated   and   did  not  react.      April  26,  delirium 


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and  opisthotonos.  Patient  became  less  noisy  after  spinal  puncture. 
April  28,  blood  count  showed  11,400  leucocytes.  April  30,  patient  spemed 
better ;  a  third  puncture  was  made.  May  4,  slight  change  ;  patient  dull, 
could  not  answer  questions.    Patient  continued  to  improve,  and  was  dis- 


50 

charged  on  May  22.  At  the  time  of  discharge  he  was  rational,  but  his 
mind  was  evidently  impaired.  Lumbar  puncture  was  made  on  April  23, 
on  the  2t)th,  and  on  April  30.  On  the  23d  two  test  tubes  were  filled  with 
a  bloody,  serous  fluid  containing  large  clots.  There  was  a  great  deal  of 
blood  and  abundant  pus  cells.  No  organisms  found  on  microscopic 
examination  or  in  cultures.  On  April  26,  15  cubic  centimeters  of  cloudy, 
yellow,  serous  fluid  removed.  Microscopically,  showed  abundant  pus  and 
epithelioid  cells  ;  diplococci  contained  in  pus  cells  and  in  cultures.  This 
puncture  made  during  an  exacerbation  of  temperature.  The  puncture 
on  April  3U  was  negative.  The  chart  shows  rise  after  entering  hospital, 
with  decline  to  sub-normal,  marked  by  exacerbations. 

Case  59.  Male,  age  twenty-nine  yeai's.  Entered  hospital  April  21. 
April  17,  chill,  headache,  general  pain  and  vomiting ;  delirious  at 
night.  On  admission,  delirious ;  head  retracted;  muscles  of  neck  stiff; 
tenderness  on  pressui-e  over  cervical  and  dorsal  vertebrae ;  j^atellar  re- 
flex absent ;  pupils  contracted.  Lumbar  puncture  made  April  22,  and 
gave  some  relief.  Died  April  23.  The  lumbar  puncture  gave  20  cubic 
centimeters  of  bloody  fluid.  Cover-slips  and  cultures  from  this  showed 
diplococci.     Post-mortem  examination. 

Case  60.  Female,  age  five  years.  Entered  hospital  April  18,  at 
3.15  A.M.  Day  before  admission,  convulsions  and  high  fever;  vomit- 
ing and  diarrhoea.  At  10.30  of  night  of  admission,  numerous  small 
hsemorrhages  into  skin  appeared  all  over  body.  On  entrance,  child  was 
moribund.  Two  minutes  after  death,  rigor  mortis  to  a  marked  degree 
in  both  legs.  Rigor  mortis  was  present  in  both  ankles  before  death. 
Rigor  rapidly  extended  to  muscles  of  neck.  Skin  all  over  body  covered 
with  i^unctate  hsemorrhages  from  the  size  of  a  pin's  head  up  to  that  of  a 
pea.  Lumbar  puncture,  Aj^ril  18,  immediately  after  death,  gave  a  puru- 
lent fluid  with  numerous  diplococci.  This  case  was  most  like  the  fulmi- 
nating cases  described  in  previous  epidemics. 

Case  61.  Male,  age  nineteen  years.  Entered  hospital  April  21. 
Three  days  before  admission,  headache  and  slight  chill ;  general  pain, 
esijecially  in  back;  vomiting.  On  admission,  slightly  irrational; 
marked  tenderness  over  mastoids  and  bcick ;  pupils  small ;  abdomen 
rigid,  tympanitic ;  tender  on  pressure  over  recti  muscles ;  purplish 
maculse  on  skin.  April  29,  complained  of  headache.  May  7,  severe 
headache  and  chill ;  broncho-pneumonia.  Patient  continued  to  improve, 
and  was  dischai'ged  June  8.  The  temperature  chai't  shows  irregular 
fever,  not  over  lUl",  then  sharp  rise  to  102°,  corresponding  to  broncho- 
pneumonia. Lumbar  puncture,  April  23,  gave  35  cubic  centimeters 
of  turbid,  slightly  yellowish  fluid.  Microscopic  examination  showed 
abundant  pus  cells  and  large  epithelioid  cells.  Diplococci  found  in  pus 
cells  in  considerable  numbers  and  sometimes  free.  Cultures  showed 
abundant  typical  development  of  diplococci. 


51 

Case  62.  Female,  age  four  and  one-half  years.  Entered  hospital 
April  20.  One  day  before  admission,  attack  began ;  no  vomiting  ;  ma- 
laise;  anorexia;  coryza,  On  admission,  restless,  delirious  and  at  times 
unconscious ;  head  retracted.  Died  April  22.  Lumbar  puncture,  post- 
mortem, gave  cloudy  fluid,  and  cultures  showed  pure  gi'owth  of  di- 
plococci. 

Case  63.  Male,  age  twenty-seven  years.  Entered  hospital  April  30, 
Nine  days  before  admission,  complained  of  severe  headache  and  pain  in 
neck,  with  vomiting.  Headache  had  not  been  constant  since,  but  there 
had  been  stiffness  of  muscles  and  retraction  of  head.  April  29,  became 
delirious.  On  admission,  unconscious,  marked  retraction  of  head  with 
rigidity  of  neck ;  conjunctivas  injected ;  pupils  equal,  moderately  di- 
lated, did  not  react;  patellar  reflex  normal.  May  1,  retraction  of  head 
less  marked ;  mental  condition  improved ;  slight  nystagmus ;  no  stra- 
bismus. May  2,  condition  more  unfavorable.  Spinal  puncture  May  2. 
May  5,  sane  mentally,  hiccoughs  ;  Cheyne-Stokes  respiration.  May  8, 
temperature  fell  to  normal.  Died  May  8.  Spinal  puncture  gave  6  cubic 
centimeters  of  cloudy  fluid,  containing  considerable  blood  Microscopi- 
cally, single  pus  cells  and  many  mononuclear  cells.  None  of  the  large 
cells  found.  On  culture,  most  of  the  tubes  sterile.  One  tube  gave  four 
colonies  of  staphylococcus  albus,  probably  a  contamination  of  the  skin. 
Puncture  negative  twelve  days  after  attack. 

Case  64.  Female,  age  three  years.  Entered  hospital  April  21.  A 
cousin  of  this  child  died  four  days  before  this  with  "  brain  fever"  in  the 
same  house  in  which  the  i^atient  was  living.  On  admission,  unconscious ; 
head  strongly  retracted ;  could  not  be  flexed  ;  convergent  strabismus  of 
both  eyes.     Continued  to  fail.     Died  April  22. 

Case  65.  Female,  age  ten  years,  Entered  hospital  April  25.  Two 
days  before  admission,  fever,  pain  in  back,  vomiting.  Lumbar  punct- 
ure April  27.  Very  cloudy  fluid.  Typical  diplococci  in  cultures. 
Died  April  29. 

Case  66.  Female,  age  twenty-eight  years.  Entered  hospital  April  26. 
Headache  and  vomiting  three  days  before  admission.  On  admis- 
sion, tenderness  over  mastoids ;  rigidity  of  neck,  without  retraction ; 
conjunctiviB  injected;  pupils  rather  small,  but  equal ;  petechiae  of  skin, 
April  20,  continuous  delirium  ;  severe  conjectivitis  in  both  eyes.  There 
was  a  sudden  rise  of  temperature  during  the  visit  of  the  physician, 
going  from  normal  up  to  105°.  Patient  comatose,  and  died  suddenly 
April  29.     Post-moi*tem  examination. 

Case  67.  Male,  age  two  and  one-half  years.  Entered  hospital  April 
24.  No  previous  history.  On  admission,  unconscious ;  eyes  open  and 
fixed ;  some  retraction  of  head.  Spinal  puncture,  on  April  26,  gave 
cloudy  fluid,  containing  pus  cells  and  diplococci.  Temperature  showed 
very  sharp  terminal  rise  to  108°. 


52 


Case  68.  INIale,  age  ten  years.  Entered  hospital  May  5.  Present 
illness  began  six  days  ago,  with  pain  in  right  leg,  followed  by  head- 
ache ;  vomiting ;  delirium  ;  three  days  after  this,  herpes  developed.  On 
entry,  herpes  about  lips  ;  muscles  at  back  of  neck  tender  and  rigid  ;  no 
tenderness  along  spine.  Blood  count  showed  1.5,000  whites.  May  7, 
seemed  better.  May  9, 1'igidity  of  neck  less  ;  less  pain  Blood  count  on 
the  15th  showed  14,000  whites ;  a  count  on  the  17th  showed  17,000 
whites.  Discharged  well  May  18.  Temperatui'e  came  down  on  day 
after  admission,  and  remained  normal. 

Case  69.  Male,  age  thirty-five  years.  Entered  hospital  May  5. 
Five  days  before  admission,  complained  of  pain  in  back  and  headache ; 
had  one  chill  the  first  day  and  one  on  day  of  admission ;  vomited  on 
three  days  before  admission.  On  admission,  pain  in  eyes,  throbbing  pain 
in  back  and  occasional  pain  in  ears;  pupils  equal,  regular  and  reacted 
alike ;  reflexes  normal ;  stifi"ness  of  neck  and  whole  back ;  slight  herpes 
and  petechise  on  nose.  May  15,  for  some  days  had  no  pain  for  several 
hours  each  day.  May  19,  marked  impi'ovement.  Discharged  well 
May  22.     Lumbar  puncture  made  May  7,  no  fluid  obtained. 


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53 

Case  70.  Male,  age  twenty-seven  years.  Entered  hospital  May  7. 
Four  days  before  admission,  began  to  have  jiain  in  arms  and  legs ;  the 
next  day,  vomited,  had  headache  and  pains  in  back ;  on  day  following 
this,  eijistaxis ;  tenderness  in  parotid  region  and  lower  down  in  neck ; 
delirium  ajjpeared.  On  entrance,  stuj^id  and  irrational ;  no  retraction  of 
head,  but  tenderness  on  jDressure  below  mastoids ;  lack  of  motion  and 
expression  on  right  side  of  face ;  herpetic  eruption  on  mouth ;  slight 
ptosis  of  right  eye,  conjunctivae  injected  ;  pupils  equal  and  reacted  nor- 
mally. May  9,  patient  was  delirious  and  noisy,  complained  of  head- 
ache, the  pain  extending  down  the  back ;  nose  bled  several  times. 
On  May  12,  marked  improvement;  at  night  of  12th,  more  delirious, 
could  not  be  kept  in  bed.  May  17,  general  condition  better ;  patient  in- 
telligent when  aroused.  A  slight  hsemorrhagic  eruption  appeared  on 
upper  part  of  abdomen.  On  the  20th,  delirious,  stupid,  not  easily 
roused ;  involuntary  micturition.  May  24,  clear  mentally.  May  27, 
jDatient  did  not  respond  to  questions ;  comj^lete  paralysis  of  right  arm 
and  leg ;  occasional  slight  nystagmus ;  eyes  turned  towards  the  left ; 
inability  to  swallow.  May  29,  cyanosis  of  face.  Died  at  2.32  p.m. 
Spinal  puncture,  May  9,  60  cubic  centimeters  of  yellow,  cloudy  fluid  ob- 
tained. On  microscopic  examination,  abundant  pus  and  ef)ithelioid  cells, 
and  a  few  lymphoid  cells.  Many  of  the  pus  cells  contained  diplococci 
in  considerable  numbei's.  Fifteen  tubes  were  inoculated  with  large 
amounts  of  the  fluid  ;  three  of  these  showed  a  growth.  On  two  of  these 
tubes  two,  and  on  one  ten,  colonies  of  typical  diplococci.  The  chart 
shows  complete  intermission  of  fever  for  two  days,  coincident  with 
marked  improvement  of  the  patient. 

Case  71.  Male,  age  two  years.  Entered  hospital  May  7.  May  5, 
suddenly  attacked  with  headache,  pain  in  abdomen  and  vomiting.  May 
6,  became  drowsy,  stupid  and  finally  unconscious.  On  admission,  per- 
sistent retraction  of  head  and  irregular  temperature,  varying  from  nor- 
mal to  106°.  Lumbar  puncture  May  7.  Fluid  cloudy,  cultures  showed 
diiDlococci  in  pus  cells.  The  child's  condition  gradually  improved. 
Emaciation  was  marked.  On  May  .30,  an  enlarged  cervical  gland  was 
noticed  ;  examination  of  throat  showed  membrane  on  both  tonsils.  Bac- 
teriological examination  showed  K.L.  bacilli.  Entered  south  depart- 
ment of  Boston  City  Hospital  June  1.  Condition  gradually  grew  worse ; 
death  on  June  3,  in  convulsions.  No  urine  passed  while  in  south 
depai'tment  hospital,  and  none  found  in  bladder  by  catheterization, 
Post-mortem  examination. 

Case  72.  Female,  age  six  years.  Entered  hospital  May  12.  Illness 
began  seven  days  before  admission  with  abdominal  pain,  fever  and 
vomiting  ;  two  days  before  admission  there  was  headache,  slight  retrac- 
tion of  head  and  delirium.  On  admission,  slight  strabismus ;  tache 
cerebrale  well  mai'ked ;  legs  flexed ;  pain  on  attempting  to  straighten 
them.  Lumbar  puncture,  May  15,  gave  cloudy  fluid  with  pure  culture 
of  diplococci.  Discharged  well  June  21.  The  temperature  chart  is  in- 
teresting, in  showing  a  very  shai'p  evening  rise,  somewhat  resembling 


54: 


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Case  73.  Male,  age  twenty-six  years.  Entered  hospital  May  21. 
Fourteen  days  before,  began  to  have  pain  in  the  back  and  head,  which  was 
continued  with  varying  severity ;  movements  of  head  painful ;  constant 
vomiting  from  the  first.  On  admission,  dull  and  slightly  delirious; 
herpes  on  lips  and  around  nose  ;  pupils  equal,  and  reacted  ;  marked  con- 
junctivitis ;  head  held  stiffly ;  motion  limited  by  pain  ;  no  tenderness  on 
pressure  over  vertebrse.  May  24,  active  delirium  ;  rigidity  of  head  and 
back  more  marked.  May  28,  less  delirious ;  no  vomiting ;  head  could 
not  be  touched  without  pain  ;  no  eye  symptoms.  June  1,  mild  delirium 
continued.  June  5,  occasional  delirium ;  rigidity  of  neck  had  in  large 
measure  passed  away.  On  June  9,  head  could  be  moved  without  pain. 
Patient  continued  to  improve,  and  on  June  21  was  dischai-ged  well. 

Case  7-4.  Female,  age  ten  years.  Entered  hospital  May  9.  Illness 
began  night  before  admission,  with  chills  and  vomiting.  On  entrance, 
high  fever;  erythematous  blotches  on  legs.  Child  rapidly  grew  worse, 
and  died  May  13.  Lumbar  puncture.  May  12,  gave  cloudy  fluid.  Cult- 
ures of  this  showed  typical  diplococci. 


Case  7.5.  Male,  age  forty  years.  Entered  hospital  May  12.  Three 
days  before  admission,  complained  of  headache  and  sore  throat;  became 
deaf  the  following  day  ;  there  was  retching,  but  no  vomiting.  On  night 
before  admission,  delirious.  On  admission,  pupils  small,  equal,  re- 
sponded slightly  to  light ;  slight  nystagmus  and  divergent  strabismus 
of  right  ej-e;  deafness;  head  stiff;  pain  on  motion;  no  retraction; 
slio-ht  tenderness  along  vertebrse  ;  reflexes  absent.     May  15,  herpes  on 


55 


lips   increased;    delirious.     May  18,  eyes   again   normal;    involuntary 
micturition.     Patient  slowly  failed,  and  died  at  7.30  pm.,  May  19. 

Case  76.  Male,  age  thirty  years.  Entered  hospital  May  17.  Patient 
was  in  bed  one  week  before  entrance,  with  severe  headache  and  pain  in 
neck,  with  limited  and  painful  motion  of  head  ;  pain  in  back  extending 
into  legs  ;  vomiting  daily  before  admission  into  hospital.  On  admission, 
head  held  fixedly ;  flexion  limited  by  pain ;  eyes  normal ;  patellar  re- 
flex normal ;   abdomen  tender.     May  20,  no  vomiting   since  entrance ; 


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headache  continued ;  patient  dull  and  quiet.  INIay  23,  slight  delirium. 
May  27,  lay  in  apparent  sttipor.  May  28,  delirious  again ;  rigidity  of 
head  and  back.  May  31,  stupor  continued  June  3,  patient  steadily 
continued  to  fail,  and  died  at  .5.30  P  M.  Lumbar  puncture.  May  19,  showed 
15  cubic  centimeters  of  a  slightly  cloudy  fluid,  which  after  some  hours 


56 

deposited  a  yellowish  clot.  The  sediment  contained  many  pus  cells, 
with  a  few  lymphoid  and  large  cells.  A  few  diplococci  found.  They 
were  occasionally  free,  usually  in  pus  cells,  several  j)airs  of  them 
grouped  about  the  nucleus.  Cultures  on  every  tube  showed  abundant 
growth  of  tyiDical  colonies.  The  chart  shows  a  fever  of  medium  degree, 
with  slight  variation,  then  fall  to  normal,  with  slight  terminal  rise. 

Case  77.  Female,  age  nineteen  years.  Entered  hosjiital  May  14. 
For  three  days  before  admission,  pain  in  head  and  neck  and  stiffness  in 
neck  and  back ;  slightly  stupid.  On  admission,  evident  pain,  some  re- 
traction of  head  ;  could  be  roused  to  answer  questions  ;  pupils  equal  and 
reacted ;  answered  questions,  but  was  dull.  May  15,  seemed  somewhat 
better,  but  became  rajDidly  cyanotic,  and  died  at  2.40  p.m.  Lumbar  punct- 
ure on  May  1-5  gave  12  cubic  centimeters  of  slightly  cloudy  fluid  with 
yellow  flocculent  precipitate.  On  microscopic  examination  abundant  pus 
cells  and  lai'ge  epitheloid  cells.  Diplococci  were  found  microscoj)ically 
and  in  cultures. 

Case  78.  Male,  age  twenty-three  years.  Entered  hospital  May  25. 
Two  weeks  before  entrance,  gradual  onset  of  temporal  headache  and 
pain  in  back  of  neck ;  vomiting ;  headache  constant.  On  admission, 
left  pupil  dilated,  reacted  sluggishly  to  light ;  slightly  enlarged  spleen ; 
patellar  reflex  absent,  other  reflexes  exaggerated  ;  faint  reddish  mottling 
over  back  and  upper  arms  :  headache  persisted  until  May  30.  May  31, 
signs  of  paralysis  on  left  side  of  face ;  eye  did  not  shut ;  corner  of 
mouth  immobile :  tongue  deviated  to  left.  June  4,  facial  paralysis ; 
frontalis  muscle  involved.  June  17,  slight  pain  on  left  side  of  head. 
June  18,  pain  more  severe,  localized  about  ear ;  mastoid  tender ;  vessels 
of  tympanum  slightly  injected.  June  19,  paracentesis.  June  20,  ear 
discharging  freely.  June  21,  tenderness  over  mastoid.  June  24,  slight 
tenderness.  June  25,  almost  no  mastoid  tenderness.  June  26,  slight  sero- 
purulent  discharge  from  ear.  June  27,  pain  in  back  of  neck.  July  2,  no 
discharge  from  ear.  July  3,  discharge  fairly  free  ;  jDain  in  neck  moder- 
ate. July  6,  no  pain  ;  slight  tenderness  ;  continuous  sero-purulent  dis- 
charge from  ear.  July  8,  comfortable.  July  10,  no  discharge ;  much 
pain  and  tenderness ;  mastoid  operation  done ;  a  large  amount  of 
purulent  material  ran  from  nose  during  the  operation,  supposed  to  be 
from  antrum.  July  16,  returned  to  medical  side.  From  the  16th  to 
the  19th,  slight  bronchitis.  July  20,  vomiting,  swelling  of  feet  and 
legs ;  mastoid  better.  July  28,  oedema  of  scrotum.  August  12,  urine 
shows  evidence  of  acute  nephritis.  August  16,  swelling  continued. 
August  18,  better.  September  3,  discharged  relieved.  On  the  19th  of 
June,  microscopic  examination  of  jdus  from  left  ear  obtained  by  para- 
centesis showed  leucocytes  and  diplococci.  June  15,  microscopic  ex- 
amination of  the  purulent  nasal  secretion  showed  a  few  intracellular 
diplococci  and  few  leucocytes.     The  dij^lococci  did  not  grow  on  culture. 

Case  79.  Male,  age  fifty-eight  years.  Entered  hospital  May  13. 
The  previous  history  of  the  patient  could  not  be  obtained,  as  he  could 


57 

speak  no  English.  On  admission,  was  semi-conscious  and  at  times 
delirious;  ptosis  of  left  eye,  left  pupil  smaller  than  right;  neither 
reacted  to  light ;  pulse  regular,  of  good  strength  and  volume  ;  patellar 
reflex  diminished  on  left  side ;  superficial  reflexes  diminished.  May 
16,  still  delirious ;  incontinence  of  urine  and  fteces ;  condition  much 
the  same  as  at  entrance.  May  19,  patient  much  weaker ;  stupor  deepened, 
and  patient  died  at  6  a.m..  May  19.  The  temperature  was  sub-normal 
while  in  hosjDital,     Post-mortem  examination. 

Case  80.  Female,  age  thirty  years.  Entered  hospital  May  21. 
Seven  daj^s  before,  headache  ;  vomited  several  times  ;  neck  not  stiff.  On 
admission,  right  pupil  slightly  larger;  both  reacted  normally;  slight 
strabismus  ;  head  retracted,  but  could  be  forced  forward  without  pain  ; 
cried  out,  groaned,  etc. ;  no  enlargement  of  spleen ;  reflexes  more 
marked  on  right  side.  Blood  count  gave  14,800  whites.  Delirious. 
May  22,  delirious ;  headache.  May  23,  no  change  in  condition.  May 
24,  picking  at  bed  clothes.  May  25,  weak,  pulse  not  so  good.  Died 
May  25.  The  temperature  was  102*^  on  entrance  ;  with  slight  remissions 
it  rose  to  105°  before  death. 

Case  81.  Female,  age  twenty-six  years.  Entered  hospital  June  14. 
Illness  began  four  weeks  ago,  with  headache ;  no  vomiting.  Patient 
stupid ;  eyes  closed ;  pupils  small ;  head  stiffly  retracted ;  no  tender- 
ness ;  res]Diration  irregular ;  patellar  reflexes  diminished ;  conjunctivte 
injected.  Blood  count  showed  10,000  whites.  June  15,  mild  delirium. 
June  19,  pulse  weak.  June  21,  mental  condition  better.  June  22, 
more  stupid ;  passed  urine  and  fasces  involuntarily.  June  24,  blood 
count  showed  14,000  whites.  July  4,  failed  all  day ;  died  at  4.45  p.m. 
Several  examinations  were  made  from  the  superior  nasal  passages.  No 
diplococci  found  on  the  early  examinations.  Examination  on  June  15 
showed  a  few  leucocytes ;  no  intracellular  organisms.  There  was  a 
high  terminal  temperature,  reaching  to  106°. 

Case  82.  IMale,  age  fifty-eight  years.  Entered  hospital  May  17. 
The  day  before  admission,  complained  of  pain  in  right  leg  and  chilly 
sensation ;  was  very  weak,  and  vomited ;  found  unconscious  at  1  p.m:. 
On  admission,  was  unconscious  and  cyanotic ;  conjunctivte  slightly  in- 
jected ;  tenderness  over  cervical  vertebrte  ;  neck  stiff,  but  no  retraction ; 
pupils  equal ;  did  not  react  alike ;  limbs  rigid ;  patellar  reflex  absent. 
Became  gradually  weaker,  and  died  at  4.50  p.ii..  May  18.  Lumbar 
puncture.  May  18,  produced  14  cubic  centimeters  of  bloody,  cloudy 
fluid,  containing  a  large  trace  of  albumin.  On  microscopic  examina- 
tion, pus  cells  with  diplococci.  Cultures  from  fluid  showed  diplococci. 
Post-mortem  examination. 

Case  83.  Male,  age  sixteen  years.  Entered  hospital  May  21.  Three 
days  before  admission,  sudden  severe  headache  in  frontal  region,  ex- 
tending down  middle  of  neck  to  middle  of  shoulders  ;  retraction  of  head, 
with  pain  on  motion.     On  admission,  conscious  ;  tenderness  over  sterno- 


58 


mastoid  and  lumbar  muscles ;   herpes  labialis :  eyes  and  reflexes  nor- 
mal.    May  24,  marked  delirium;  retraction  of  head  less  marked.     May 

26,  delirium  increased ;  frequent 
vomiting.  May  27,  somewhat  bet- 
ter. May  29,  i^atient  became  worse, 
and  died  at  12.45. 

Case  84.  Female,  age  thirty- 
one  years.  Entered  hospital  May 
22.  Three  days  before  entrance, 
l^ain  in  head  and  back  of  neck,  and 
vomiting ;  became  unconscious. 
On  admission,  pupils  equal ;  con- 
vergent strabismus  on  right  side ; 
head  partially  retracted ;  no  ten- 
derness over  cervical  vertebrse ; 
spleen  not  enlarged ;  diminished 
patellar  reflex.  Blood  count 
showed  18,000  whites.  May  23, 
still  unconscious ;  quiet  most  of 
the  time,  groaned  if  moved;  re- 
traction of  head  more  marked  than 
at  entry.  Died  May  24.  Temper- 
ature chart  shows  steady  rise  from 
time  of  admission  to  death.  Post- 
mortem examination. 

Case  85.  Male,  age  twenty- 
five  years.  Entered  hospital  May 
22.  Two  days  before  admission, 
felt  tired,  remained  in  bed,  com- 
plained of  general  tendernpss  of  scalp  and  soreness  of  head.  On  May 
21,  complained  of  numbness,  and  became  delirious  in  the  evening.  On 
entrance,  semi-conscious,  dull  and  restless ;  pupils  of  equal  size,  and 
reacted  alike  ;  patellar  reflex  normal ;  no  rigidity  of  extremities  ;  some 
stiffness  of  neck,  which  was  not  tender  on  pressure.  On  the  26th,  con- 
vergent strabismus  of  both  eyes  Lumbar  jjuncture,  May  24,  gave  about 
60  cubic  centimeters  of  clear,  serous  fluid,  which  deposited  a  yellow  viscid 
sediment.  It  contained  many  piis  cells  and  a  few  large  mononuclear 
cells  with  vesicular  nuclei.  There  were  few  large,  flat  diplococci  in  the 
pus  cells,  and  cultures  gave  abundant  growth  of  typical  dijDlococcus 
colonies  In  this  case  thei'e  was  extensive  diplococcus  iDueumonia.  The 
chart  shows  a  terminal  rise  of  temperature.     Post-mortem  examination. 


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Case  86.  Female,  age  thirteen  years.  Entered  hospital  May  24. 
Two  days  before  admission,  vomited  ;  this  was  followed  by  pain  in  neck, 
with  retraction.  Night  before  admission,  unconscious ;  lay  on  right 
side,  with  her  face  buried  in  pillows.  Slight  retraction  of  head,  with 
tenderness  in  back  of  head  and  neck ;  herpes  labialis ;  slight  bulging 


59 


of  left  eye  ;  slight  nystagmus  ;  pupils  normal.  May  25,  small  purplish 
spots  in  right  axila.  May  26,  quieter;  not  easily  aroused;  pulse  rapid 
and  feeble  ;  unconsciousness  continued.     Death  at  12.46  p.m. 


Case  87.  Male,  age  thirty-five  years.  Entered 
hospital  May  30.  Six  days  before  admission,  com- 
plained of  pain  all  over  body ;  four  days  before 
had  chill ;  headache  and  pain  in  neck  and  back 
had  been  constant  and  severe ;  vomited  every 
day  ;  several  times  had  nose-bleed.  On  admission? 
pupils  and  reflexes  normal.  June  2.3,  headache ; 
pain  and  rigidity  in  neck  and  back.  June  2,  spinal 
puncture.  June  7,  patient  not  so  well ;  seemed 
dull.  June  11,  patient  had  evidently  failed  ;  he  was 
dull,  unresponsive,  and  had  been  delirious  for  one 
or  two  nights ;  neck  held  rigidly.  June  15  to 
June  23,  the  condition  continued.  On  the  26th, 
chill ;  temj^erature  and  pulse  rose,  and  death  oc- 
curred at  11.45  P.M.  Spinal  puncture  made  June 
2.  About  20  cubic  centimeters  of  cloudy  serous 
fluid  removed.  Examination  showed  abundant  pus 
and  large  epithelioid  cells.  A  few  diplococci  wei'e 
found  in  the  pus  cells.  Cultures  gave  abundant 
typical  growth.  There  is  complete  intermission 
in  temperature  on  June  11,  12  and  13,  coincident 
with  evident  failure  of  patient. 

Case  88.  Male,  age  seventeen  years.  Entered 
hospital  May  30.  Had  had  weakness  and  general 
m.alaise  four  days  before  admission  On  day  be- 
fore admission,  complained  of  obstruction  of  nose^ 
and  frontal   headache   and  vomiting ;    on  day  of  bj.j.  c^gg  35. 

admission,  became   unconscious.     On    admission, 

complained  of  intense  pain  in  back  and  neck  and  across  forehead; 
stiffness  of  muscles  of  neck,  slight  retraction  of  head ;  tenderness 
over  mastoid  region;  pupils  equal  and  reacted  alike.  May  31,  slightly 
conscious ;  marked  convergent  strabismus  of  left  eye.  Died  at  9.40. 
Lumbar  puncture,  made  just  after  death,  gave  20  cubic  centimeters  of  a 
rather  thick,  bloody  fluid,  in  which  a  thick  clot  formed  after  six  hours. 
Microscopic  examination  showed  abundant  pus  cells  and  many  large 
epithelioid  cells  with  vesicular  nuclei,  occasionally  containing  enclosed 
pus  cells.  A  few  flattened  diplococci  were  found  within  the  pus  cells 
grouped  about  the  nuclei.  Cultures  gave  an  abundant  pure  growth  of 
diplococci. 

Case  89.  Male,  age  thirty-seven  yeai's  Entered  hospital  May  31. 
On  May  27,  complained  of  pain  in  small  of  back  and  legs;  there  was 
severe  headache  for  three  days,  and  for  two  days  he  was  unconscious 
for  a  short  time ;  a  great  deal  of  vomiting.     On  admission,  dull  and 


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stupid,  but  answered  questions  fairly  well ;  complained  of  pain  across 
forehead  and  back  of  neck ;  stiffness  of  neck ;  head  held  rigidly,  pain 
upon  rotation ;  not  retracted ;  pupils  equal ;  slightly  contracted  and 
reacted  slowly ;  patellar  reflex  normal.  On  June  4,  patient's  general  con- 
dition improved ;  no  delirium.  On  this  day  had  a  chill,  and  pneumonia 
appeared.  Cultures  taken  from  the  nose  showed  no  diploeocci.  June 
5,  well-developed  pneumonia ;  patient  delirious,  noisy,  violent  and  re- 
quired restraint.  June  7,  patient  weaker  and  cyanotic ;  failed  rapidly, 
and  died  at  10.30  a.m.  The  appended  chart  shows  a  sharp  rise,  coinci- 
dent with  the  development  of  the  pneumonia.    Post-mortem  examination. 


Case  90.  Male,  age  thirty-three 
years.  Entered  hospital  July  5.  Ill- 
ness began  five  weeks  before  ad- 
mission, with  severe  pain  in  foi'e- 
head.  On  night  before  admission,  in- 
tense pain  on  left  side  of  forehead. 
While  at  drug  store,  where  he  went 
to  consult  a  doctor,  had  an  attack  of 
dizziness  and  vomiting.  On  admis- 
sion, face  flushed ;  eyes  injected ; 
walked  with  difficulty ;  severe  pain ; 
marked  rigidity ;  slight  divergent 
strabismus ;  no  stiffness  of  neck,  no 
tenderness  ;  arms  rigid  ;  abdomen  re- 
tracted ;  patellar  reflex  active.  Blood 
count  showed  22,000  whites.  July  6, 
temperature  continued  to  rise  ;  uncon- 
scious. Examination  of  nasal  secre- 
tion from  upper  sinuses  showed  pus 
cells  enclosing  diploeocci.  July  7, 
still  unconscious ;  conjunctivae  more 
injected.  Died  July  7.  The  temper- 
ature in  this  case  is  remarkable, 
showing  a  gradual  increase  from  time 
of  entry  into  hospital,  reaching  109° 
six  hours  before  death.  Post-mortem 
examination. 


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Case  91.  Male,  age  twenty-seven  years.  Entered  hospital  June  10. 
One  week  before  entry,  chill,  followed  by  headache,  nausea  and  vomit- 
ing. On  admission,  stiffness  of  head  ;  herpes  ;  soreness  in  all  the  limbs  ; 
pain  on  pressure  over  mastoids ;  eyes  normal ;  patellar  reflex  absent ; 
knee  joints  sore  and  stiff.  June  21,  blood  count  showed  15,800  leuco- 
cytes. June  26,  condition  improved.  ,  Blood  count,  9,800  leucocytes. 
July  2,  intense  headache,  neck  stiff,  but  more  comfortable.  July  9,  pain 
in  head,  mild  delirium.  July  30,  patient  was  delirious  ;  knee  very  painful 
and  swollen  ;  much  exudation  present.  August  9,  patient  up  and  about ; 
knee  better.     Dischai-ged  August  11. 


61 

Case  92.  Male,  age  twenty-nine  years.  Entered  hospital  June  8. 
Four  days  before  admission,  complained  of  jjain  in  laead  and  abdomen  ; 
three  days  before,  screamed  and  threw  himself  about ;  day  before  ad- 
mission, became  suddenly  deaf.  On  admission,  eyes  normal ;  stiflfness 
of  neck  and  pain  on  motion  ;  apparent  total  deafness  ;  mental  condition 
dull  and  confused  ;  apparently  in  much  pain, but  could  not  definitely  locate 
it.  June  10,  marked  herpes  labialis.  June  14,  still  deaf,  but  heard 
better  than  at  entry,  June  16,  chill.  June  18,  held  head  stiffly,  and 
complained  of  pain  in  head  and  neck.  June  22,  delirious  for  two  nights. 
June  26,  bloody,  purulent  discharge  from  left  ear.  June  30,  was  losing 
strength  and  becoming  more  stupid.  Died  July  4.  Lumbar  puncture, 
June  9,  gave  12  cubic  centimeters  of  a  cloudy,  serous  fluid  with  thick, 
yellow,  tenacious  sediment,  much  fibrin,  many  pus  cells,  few  endothelial 
cells  ;  very  few  pairs  of  flattened  diplococci  in  jjus  cells.  Cultures  gave 
typical  diplococci. 

Case  93.  Male,  age  twenty-four  years.  Entered  hospital  June  6. 
Two  days  before  admission,  chill,  with  headache  and  vomiting ;  great 
prostration.  On  examination,  head  not  retracted ;  pupils  dilated  and 
reacted  ;  nystagmus  ;  pain  on  attempting  to  flex  head  ;  rigidity  of  mus- 
cles at  back  of  neck ;  patellar  reflexes  diminished ;  tremor  of  hands ; 
legs  not  I'igid ;  moi'e  or  less  restless ;  vomiting.  Blood  count  showed 
10,000  whites.  June  8,  herpes  developed.  June  9,  blood  count  showed 
15,000  whites.  June  10,  16,000  whites.  Pupils  at  times  unequal ;  di- 
vergent strabismus  of  left  eye ;  herpes  marked  on  upper  part  of  jaw. 
June  11,  condition  about  the  same.  June  13,  whites  same  count.  June 
17,  quieter ;  slept.  Blood  count  the  same.  June  18,  general  condition 
not  so  good.  June  19,  diminished  leucocytes,  12,000  whites.  June  20, 
condition  the  same ;  leucocytes  13,000.  June  23,  16,000.  June  25, 
10,000.  July  7,  stiffness  of  left  knee ;  no  pain.  July  8,  left  knee 
swollen,  fluctuating,  patella  floating.  Condition  in  knee  continued  to 
impi'ove.  Patient  discharged  well  July  14.  Examination  of  nasal 
secretion  was  made  June  10,  and  showed  diplococci  decolorized  by 
Gram  inside  of  leucocytes.  June  15,  showed  numerous  Gram  decolor- 
izing diplococci  in  leucocytes.  June  26,  none  found.  The  chart  is  in- 
teresting, as  showing  a  considerable  temperature  on  entry  into  hospital. 
The  temperature  remained  up  until  June  19,  when  there  was  a  fall,  with 
another  rise  on  the  22d,  after  which  it  remained  normal. 

Case  94.  Female,  age  thirty-two  years.  Entered  hospital  June  16. 
Eleven  days  before  admission,  had  sudden  severe  headache,  with  pain  in 
occipital  region ;  more  or  less  nausea  and  vomiting  began  soon  after 
headache  ;  aftei-wards  pain  in  lumbar  region  and  in  hip  developed.  Day 
before  admission,  became  hard  of  hearing.  No  herpes ;  no  aj)petite ; 
never  unconscious  On  admission,  looked  dull ;  cheeks  flushed  ;  pupils 
irregular,  reacted  equally ;  somewhat  deaf;  complained  of  pain  in  occi- 
pital region  when  head  was  flexed  ;  no  tenderness  in  back  of  head ;  no 
rigidity.  Blood  count  showed  12,000  whites.  June  18,  had  ringing 
and  drumming  in  ears ;  patient  continued  worse ;  somewhat  delirious. 


62 


June  20,  right  pupil  contracted ;  did  not  react.  Died  June  20.  Exam- 
ination of  nasal  secretion  on  June  18  and  19  showed  diplococci  decol- 
orized by  Gram,  within  leucocytes. 


Case  95.  Male,  age  thirty-one  years.  Entered  hospital  June  12. 
Three  days  before  admission,  pain  all  over  body ;  face  flushed  ;  frontal 
headache ;  pain  in  legs ;  vomiting ;  on  entry,  eyes  normal ;  herpes  of 
lower  lip  and  right  nostril ;  spleen  enlarged.  June  1.3,  less  headache. 
June  14,  delirious.  June  15,  quieter.  June  16,  irrational.  June  21, 
increase  of  temperature,  and  pain  back  of  neck  June  24,  severe  pain 
in  back  and  neck,  not  relieved  by  morphia  by  mouth,  which  continued 
unabated  until  July  4.  July  4,  area  of  splenic  dulness  increased.  July  5, 
mild  delirium  ;  tremor  of  hands  ;  slight  headache.  July  7,  no  morphia 
for  sevei'al  days,  July  8,  did  not  recognize  wife;  did  not  respond 
quickly  to  questions  ;  tremor  of  hands  more  marked.  July  9,  died  sud- 
denly. ^Examination  of  nasal  secretion,  July  8,  showed  leucocytes  and 
diplococci.  Temperature  extremely  irregular,  never  very  high.  No 
terminal  rise. 


Case  96.  Female,  age 
sixteen  years.  Entered 
hospital  June  12.  Two 
days  before  admission, 
headache,  vomiting,  and 
pain  in  head  and  back. 
On  admission,  slight  de- 
lirium ;  retraction  of  head ; 
tenderness  over  back  of 
neck ;  herpes  labialis  ;  eyes 
normal ;  patellar  reflex 
diminished.  June  15,  pa- 
ralysis of  left  side  of  face 
developed ;  herpes  on  both 
ears  and  sides  of  neck  ;  no 
delirium ;  patellar  reflex 
absent;  left  knee  swollen 
and  painful.  June  19,  eyes 
injected ;  no  complaint  of 
pain ;  general  condition 
much  worse.  Died  sud- 
denly June  24.  The  chart 
shows  an  exceedingly 
irregular  curve,  with  a  gen- 
eral downward  tendency. 
The  pulse,  equally  irreg- 
ular, gradually  ascends. 


Case  97.     Female,  age  thirty  years.     Entered  hospital  June  11.     No 
history  could  be  obtained,  as  patient  was  semi-conscious  on  admission, 


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and  had  no  friends.  Patient  resisted  examination.  Pupils  regular  and 
small,  and  did  not  react ;  held  head  stiffly,  turned  toward  the  left ;  no 
marked  pain  on  movement  of  head ;  no  tenderness  along  spine ;  no 
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flexion  ;  pupils  equal  and  reacted  slowly ;  some  pain  in  legs  and  back. 
June  18,  mind  still  clear ;  exti'eme  pain  in  back  and  limbs.  Died  sud- 
denly at  8. 30  A.M.,  June  19.  Spinal  puncture  made  post-mortem ;  5 
cubic  centimeters  of  a  bloody  fluid  obtained,  which  showed  abundant 
pus  with  diplococci  in  pus  cells.  The  organisms  were  usually  in  single 
pairs,  two  pairs  being  found  in  only  two  cases.  The  organisms  did  not 
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Case  99.  Male,  age  t^venty-four  years.  Entered  hospital  June  28. 
Seven  days  before  admission,  chill  and  vomiting ;  since  then,  two  more 
chills.  Complained  of  severe  headache  in  back  of  head,  pain  extended 
down  spinal  column.  On  admission,  stiftness  and  limited  motion  of 
head ;  tenderness  on  pressure  in  cervical  and  lumbar  region.  Blood 
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14,200.  July  2,  patient  in  mild  delirium,  but  seemed  to  be  free  from 
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64 

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shows  an  irregular,  generally  high,  temperature,  with  one  marked  inter- 
mission. There  is  a  gradual  increase  in  the  pulse,  which  shows  no 
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Case  100.  Male,  age  twenty-six  years.  Entered  hospital  June  29. 
Week  before  entiy,  headache,  vomiting,  no  chill ;  pains  in  back  of  neck  ; 
became  stupid  two  days  before  entry.  On  entry,  expression  dull,  stupid  ; 
right  pupil  larger;  both  reacted  alike;  divergent  strabismus  more 
marked  on  right  side.  July  1,  stupid;  muttering  delirium;  herpes  on 
forehead  ;  nystagmus ;  reflexes  more  active  on  right  than  left.  Steady 
decline ;  died  at  6.20  p.m.  The  temperature  shows  a  continual  rise  until 
death,  reaching  108^".  Examination  of  nasal  secretion,  July  1,  showed 
some  diplococci  decolorized  by  Gram,  in  leucocytes.  Post-mortem 
examination. 


65 

Case  101.  Female,  age  nine  months.  Entered  hospital  July  4. 
Illness  began  twelve  days  before  admission,  with  diaiThoaa  and  fever. 
Child  held  head  backwards.  Discharge  from  eyes  developed.  On  ad- 
mission, sero-pm-ulent  secretion  from  eyes ;  pupils  contracted ;  con- 
vergent strabismus ;  child  lay  with  head  retracted ;  rigid ;  no  herpes. 
July  7,  hyperi^emic  spots,  with  htemorrhages  on  right  side  of  face  and 
temple ;  convulsive  movements  more  marked,  as  well  as  retraction  of 
head ;  almost  opisthotonos ;  no  herpes ;  condition  not  much  altered. 
July  22,  blood  count  showed  17,800  whites.  Petechi^e  had  disajDiDeared. 
July  23,  vomiting  ;  purulent  discharge  from  right  ear.  Examination  of 
pus  from  ear  showed  diplococci  decolorizing  by  Gram.  Death,  July  23. 
July  6,  examination  of  nasal  secretion  showed  a  few  diplococci  in  pus 
cells.  On  examination  on  July  8,  they  were  absent.  Examination  of 
conjunctival  pus,  July  8,  showed  no  diplococci.  The  temperature  of 
this  case  is  exceedingly  irregular,  running  a  high  course  throughout. 

Case  102.  Male,  age  six  years.  Entered  hospital  June  30.  Illness 
began  with  vomiting ;  retraction  of  head.  Continued  to  improve.  Dis- 
charged well  August  3. 

Case  103.  Male,  age  fifty-two  years.  Entered  hospital  July  7.  No 
previous  history  obtained,  except  that  patient  said  he  had  been  sick  for 
one  week  before  admission.  On  admission,  stiffness  of  neck ;  motion 
limited  by  pain  ;  tenderness  to  pressure  in  upper  cervical  region  ;  spas- 
modic twitching  of  arms ;  eyes  normal,  with  the  exception  of  slight  con- 
junctivitis ;  reflexes  exaggerated.  Blood  count,  July  8,  showed  8,000 
whites.  Blood  count,  July  11,  showed  18,-100  whites.  July  11,  patient 
became  noisy,  then  stupid,  the  stupor  continuing  until  death.  Post- 
mortem examination. 

Case  104.  Female,  age  forty-six  years.  Entered  hospital  July  12. 
Ten  days  before  admission,  had  nausea  and  vomiting ;  pain  in  back  of 
neck  and  general  weakness  ;  complained  of  double  vision  ;  pain  in  neck 
somewhat  relieved  when  head  was  retracted.  On  admission,  was  con- 
scious and  rational ;  tenderness  in  back  of  neck  ;  rotation  and  flexion  of 
head  painful ;  slight  droojaing  and  loss  of  exj^ression  on  left  side  of  face  ; 
mouth  drawn  to  right;  herpes  labialis ;  convergent  strabismus;  pupils 
normal ;  patellar  reflex  absent ;  petechise  over  abdomen.  Blood  count 
showed  19,600  leucocytes.  July  14,  patient  still  complained  of  pain  in 
neck,  and  weakness.  July  15,  the  paresis  less  marked,  and  less  diplopia. 
July  18,  patient  better ;  paralysis  almost  disappeared.  July  20,  mental 
derangement ;  patellar  reflex  still  absent.  July  24,  patient  weaker ;  de- 
lirious most  of  the  time.  Death,  July  25.  The  appended  chart  shows 
an  inverse  curve  of  pulse  and  temperatui'e.     Post-mortem  examination. 

Case  105.  Male,  age  thirty-eight  years.  Entered  hospital  July  5. 
No  history  could  be  obtained  from  patient,  save  that  he  had  worked 
until  three  days  before  admission.  On  admission,  his  aspect  was  dull ; 
there  was  herpes  labialis ;  eyes  normal ;  patellar  reflex  slight  on  left, 


66 


absent  on  right  side.  July  8,  blood  count  showed  15,600  leucocytes. 
July  16,  by  spinal  jjuncture  a  small  amount  of  cloudy  fluid  obtained, 
containing  pus  cells  and  diplococci.  July  21,  patient  in  mild  delirium 
since  July  16.  At  times  he  was  quite  rational ;  at  others  stupid.  July  25, 
patellar  reflex  absent.  July  30,  no  change  from  last  note ;  patient  still 
continued  stupid.  The  condition  became  somewhat  better,  pulse  and 
temperature  became  normal,  and  patient  left  hospital  August  31  with 
marked  mental  impairment. 


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Case  106.  Female,  age  twenty-seven  years.  Entered  hospital  July  6. 
On  July  3,  patient's  child  died  of  cei-ebro-spinal  meningitis,  child  being 
ill  for  twelve  hours.  After  this  she  appeared  dazed  and  at  times 
delirious.  In  the  evening  she  complained  of  pain  in  the  back  of  neck ; 
began  to  vomit,  which  continued  for  twenty-four  hours  On  admission, 
patient  unconscious ;  joints  of  wrists  and  ankles  swollen,  red  and  pain- 
ful ;  head  jjainf ul  on  iiiotion  ;  pain  on  pressure  on  calves  and  thighs. 
July  7,  marked  divergent  strabismus  Blood  count  showed  29,400  whites. 
July  9,  blood  count  showed  14,000  whites.  Patient  much  better ;  neck 
less  stiff;  no  strabismus.  July,  19,  blood  count  showed  19,400  whites. 
Patient  discharged  well  August  11.  Lumbar  puncture,  July  7,  gave 
small  amount  of  cloudy  fluid  which  contained  pus  cells  and  diplococci. 

Case  107.  Male,  aged  thirty-two  years.  Entered  hospital  July  26. 
On  July  4,  began  to  have  severe  headaches  ;  no  pain  or  stiffness  in  back 
of  head  or  neck  ;  general  pain  in  body  ;  weakness,  loss  of  appetite  and 
drowsiness  ;  no  vomiting.  On  admission,  semi-conscious  and  restless ; 
eyes  rolled  upwards ;  reflexes  normal ;  no  herpes ;  pulse  full,  strong 
and  slow;  jDatellar  reflex  absent;  no  retraction  of  head.  July  27, 
blood  count  showed  11,500  leucocytes.  July  30,  patient  sank  gradually 
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See  Case  108. 


68 


and  faeces,;  retraction  of  head  appeai'ed,  and  at  times  amounted  to 
opisthotonos ;  weakness  increased ;  death  occurred  at  4.15  p.m.  Post- 
mortem examination,  which  showed  a  mixed  infection  with  tuberculous 
meningitis. 

Case  108.  Male,  age  twenty-six  years.  Entered  hospital  July  6. 
Two  days  before  admission  began  to  vomit,  and  complained  of  head- 
ache. On  admission,  unconscious  ;  eyes,  normal ;  head  held  rigidly,  with 
slight  retraction  at  times  ;  pain  on  motion.  Blood  count,  July  7,  showed 
16,400  whites.  July  14,  slight  irregularity  of  pupils.  July  18,  stupor 
more  marked.  July  22,  profound  stupor;  head  retracted;  eyes  and 
mouth  j)artly  open  ;  corneal  reflex  gone.  July  26,  stupor  deepened,  until 
the  morning  of  the  26th,  when  temperature  dropped  and  he  seemed 
better.     July  28,  marked  improvement,  which  lasted  until  August  1. 


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August  7,  temperature  had  remained  normal  for  three  days  ;  recognized 
nurse,  but  was  not  clear  mentally.  August  11,  pulse  weaker ;  respirations 
increased  in  rapidity ;  patient  thought  to  be  dying  ;  next  morning,  better. 
August  15,  patient  increased  in  strength ;  mild  delirium.  August  17, 
blood  count  gave  13,400  corpuscles.  August  19  to  August  22,  con- 
tinued to  improve  physically  and  mentally;    bed  sores   over   sacrum. 


69 

The  imprnvcment  continued,  and  at  this  time,  September  20,  the  patient 
is  still  in  the  ward,  but  his  general  condition  is  good.  The  apjjended  tem- 
perature and  pulse  curve  shows  the  extreme  irregularity  which  may  be 
seen  in  a  chronic  case. 

Case  109.  Female,  age  thirty-two  years.  Entered  hospital  July  24. 
On  the  22d,  began  to  vomit,  and  complained  of  severe  headache ;  vomit- 
ing continued  until  the  morning  of  admission.  The  headache  was  sevei-e, 
with  darting  pains  in  back  of  neck;  was  unconscious  part  of  the  time  ; 
eyes  normal ;  reflexes  normal ;  tenderness  over  spinous  processes  of 
cervical  and  dorsal  vertebrae.  Blood  count,  July  25,  showed  13,800 
whites.  July  28,  herpes  labialis  developed.  Had  been  in  great  pain^ 
since  entry,  but  was  somewhat  better.  Blood  count,  July  29, 7,40U  whites. 
Patient  became  gradually  better,  and  was  dischai'ged  well  August  14. 

Case  110.  Male,  age  three  and  a  half  yeai's.  Entered  hospital  Sep- 
tember 12.  Unconscious  on  day  of  admission.  Died  September  15. 
Retraction  of  head.  This  case  is  interesting,  as  showing  a  well-marked 
terminal  rise  of  temperature,  which  reached  109.7°  just  before  death. 
Post-mortem  examination. 

Case  111.  Male,  age  thirty-five  years.  Entered  hospital  Septem- 
ber 18.  Two  days  before  admission,  complained  of  headache,  vomiting 
and  diarrhoea.  On  admission,  unconscious  ;  face  flushed  ;  expression 
anxious  ;  head  turned  slightly  to  the  left ;  mouth  drawn  to  left ;  respi- 
ration labored  and  noisy  ;  turning  of  head  to  right  resisted  ;  no  retrac- 
tion of  head ;  no  evidence  of  tenderness  to  pressure  over  vertebrae  ; 
pupils  reacted  alike ;  slight  dulness  posteriorly  in  both  lungs,  more 
marked  on  right  side  ;  respiration  noisy ;  loud  rales  heard '  everywhere  ;• 
patellar  reflex  normal ;  considerable  loss  of  power  both  of  arm  and  of 
leg  on  right  side.  September  19,  area  of  dulness  of  right  base  greater;, 
bronchial  respiration  and  moist  rales  :  right  pupil  larger  than  left ;  a 
divergent  strabismus  developed.  Remained  unconscious  until  death, 
"which  occurred  on  19th.  Lumbar  puncture  made  on  19th,  shortly  before 
death,  gave  a  considerable  amount  of  slightly  cloudy  fluid,  which  in  the 
course  of  twelve  hours  developed  a  slight  amount  of  whitish  yellowish 
sediment  and  a  considerable  amount  of  fibrin,  which  formed  a  definite 
layer  thi'ough  the  entire  tube.  Microscopic  examination  of  the  fluid 
showed  the  sediment  composed  of  polynuclear  pus  cells,  with  numbers- 
of  diplococci  within  them.     Post-mortem  examination. 


70 


BACTERIOLOGY. 

The  aetiology  of  the  disease  has  been  involved  in  obscurity 
until  quite  recently.  Notwithstanding  the  numerous  investiga- 
tions made  with  the  view  of  ascertaining  the  particular  micro- 
organism which  could  be  regarded  as  a  causative  agent,  it  is 
only  recently  that  such  an  organism  has  been  discovered  and 
its  causal  relation  to  the  disease  been  proven. 

The  first  description  of  an  organism  which  might  be  con- 
sidered as  the  diplococcus  intracellularis  was  given  by  Leichten- 
stern^  in  his  first  paper  on  meningitis  in  which  he  describes 
the  first  cases  seen  in  the  epidemic  in  Cologne.  He  found  in 
the  exudation  in  the  meninges  a  few  cocci,  sometimes  single, 
sometimes  in  groups  similar  in  arrangement  to  gonococci,  enclosed 
in  white  corpuscles.  Schwabach  found,  in  pus  from  a  case  of 
otitis  media  secondary  to  meningitis,  diplococci  in  the  pus  cells. 
It  is  probable  that  in  this  case  also  the  organism  was  the  dip- 
lococcus intracellularis.  In  1887  Weichselbaum^*^  described  a 
peculiar  form  of  micrococcus,  resembling  the  gonococcus,  which 
he  found  in  six  cases  of  acute  cerebro-spinal  meningitis.  "When 
these  cases  appeared  the  disease  was  not  prevailing  in  Vienna 
in  epidemic  form,  although  there  was  at  the  time  an  epidemic 
in  Mailberg,-'^  in  lower  Austria.*  The  organism  described  by 
Weichselbaum  was  a  diplococcus  occurring  almost  solely  within 
the  cells.  It  grew  best  on  agar-agar.  In  pure  culture  it 
formed  a  grayish- white,  rather  viscid  growth,  and  the  single 
colonies  often  appeared  to  be  formed  of  small  confluent  masses. 
It  would  not  grow  at  room  temperature,  and  died  quickly,  so 
that  new  cultures  had  to  be  made  every  two  days.  In 
cultures  the  organisms  occurred  singly,  in  pairs  and  in 
tetrads.  Both  in  cultures  and  in  the  tissue  they  were  de- 
colorized by  the  Gram  stain.  They  were  not  easily  demonstrated 
in  sections  of  the  meninges,  and  in  most  cases  but  few  organ- 
isms were  found.      Weichselbaum  inoculated  mice,  guinea-pigs, 

*  Widerhoferi22  reported  seven  cases  of  cerebro-spinal  meningitis  in  children  in 
Vienna  in  1885,  just  before  the  cases  seen  by  "Weichselbaum^-".  The  histories  of 
the  cases  given  by  Widerhofer  and  "Weichselbaum  coincide  with  the  epidemic  form. 


71 

rabbits  and  dogs  with  pure  cultures  of  the  organism.  Subcu- 
taneous inoculations  were  without  result,  but  inoculation  in  the 
pleural  or  peritoneal  cavities  proved  fatal  to  guinea-pigs  and 
rabbits  in  from  one  to  four  days.  In  these  serous  mem- 
branes, inflammation  with  sero-flbrinous  exudation  was  pro- 
duced. He  produced  meningitis  and  encephalitis  in  dogs  by 
inoculating  them  directly  in  the  meninges.  He  found  the 
organism  not  only  in  the  meninges  in  all  six  of  his  cases, 
but  also,  in  one  case,  in  foci  of  broncho-pneumonia  in  the 
luDgs.  The  plate  which  accompanies  the  article  of  Weich- 
selbaum  gives  a  very  correct  representation  of  the  organ- 
ism, showing  the  irregular  and  swollen  forms  which  are 
sometimes  found.  He  called  the  organism  the  diplococcus 
intracellularis  meningitidis.  Goldschmidt^^^  found  the  diplo- 
coccus in  a  case  of  acute  meningitis  in  a  child  of  four 
months.  His  description  of  the  morphology  and  cultural 
peculiarities  of  the  organism  agrees  essentially  with  that 
given  by  Weichselbaum.  Netter'*  investigated  twenty-five  cases 
of  meningitis,  with  reference  to  the  bacteria  present,  and  found 
the  diplococcus  intracellularis  in  two  of  these  cases. 

There  is  no  other  mention  made  of  this  organism  until  1895, 
when  the  most  important  confirmation  of  "Weichselbaum's 
investigation  appeared.  Jager^^^  described  the  diplococcus  in 
twelve  cases  of  epidemic  cerebro-spinal  meningitis  occurring  in 
the  garrison  in  Stuttgart.  His  description  of  it  agrees  essen- 
tially with  that  of  Weichselbaum,  with  the  exception  that  he 
says  a  capsule  was  sometimes  found  around  the  organisms,  and 
that  cover-slips  made  from  the  cultures  could  be  stained  with 
Gram.  In  cultures  there  was  some  tendency  for  the  organism 
to  grow  in  streptococcus  form,  and  a  fine  line  running  longitu- 
dinally could  be  made  out  along  the  chain.  He  calls  attention 
to  the  very  slight  amount  of  exudation  which  he  found  in  most 
of  the  cases.  The  number  of  organisms  varied  with  the  amount 
of  exudation,  being  most  numerous  where  the  exudation  was 
most  abundant.  In  only  two  cases  was  there  a  microscopic 
examination  made  of  the  meninges  and  in  these  the  organisms 
were  found  in  small  numbers. 


72 

Heubner^^^  found  the  diplococcus  in  nine  typical  cases  of 
cerebro-spinal  meningitis  in  the  fluid  obtained  by  lumbar 
puncture.  He  produced  acute  meningitis  in  goats  by  injecting 
pure  cultures  of  the  organism  into  the  spinal  canal.  His 
experiments  on  other  animals  were  negative.  There  were  other 
cases  of  meningitis  in  Berlin  at  the  time  when  Heubner  made  his 
report.  In  six  of  Heubner's  cases  the  diagnosis  made  by  spinal 
puncture  was  confirmed  by  post-mortem  examination. 

Holdheim^^  gives  the  result  of  spinal  puncture  in  four  cases  of 
meningitis.  In  all  of  these  cases  the  organisms  were  obtained. 
Two  of  the  cases  died,  and  the  organisms  were  found  on  post- 
mortem examination.  He  confirms  Jager's  description  of  the 
streptococcus  form  and  the  longitudinal  line  found  in  this. 

Peterson^"  investigated  an  epidemic  of  the  disease  in  Berlin  in 
1895  and  1896.  In  twelve  post-mortem  examinations  he 
found  the  diplococcus  in  the  exudation  in  the  spinal  canal. 
Furbringer^^^  found  the  diplococcus  intracellularis  in  the  menin- 
geal exudation  of  an  individual  who  had  acute  gonorrhoea  at  the 
same  time.  The  two  oi'ganisms  were  so  similar  in  appearance 
that  he  thought  they  might  be  the  same,  but  cultures  showed 
the  difference.  Kischensky^^  reports  a  case  of  cerebro-spinal 
meningitis  in  which  he  found  the  diplococcus  in  the  meninges  and 
in  hsemorrhagic  foci  in  the  lungs.  This  article  is  valuable  for  the 
histological  description  of  the  lesions.  Kister^^^  obtained  the 
organisms  in  two  cases  from  fluid  removed  by  spinal  puncture. 
He  found  some  difficulty  in  growing  the  organisms  on  agar-agar, 
and  obtained  the  best  growth  on  blood-serum  agar.  Sub- 
cutaneous inoculation  was  without  result,  but  animals  inoculated 
in  the  pleura  or  peritoneum  died  in  from  four  to  six  days. 
Stoeltzner^"^  found  the  diplococcus  in  the  fluid  obtained  by  lum- 
bar puncture  in  a  sporadic  case  of  meningitis  in  a  child  two  and 
one-half  years  old.  The  fluid  was  cloudy,  and  contained  the 
diplococci  enclosed  in  pus  cells.     The  child  recovered. 

Finkelstein^^  found  the  organism  on  post-mortem  examination 
of  one  case  which  died  and  in  the  fluid  withdrawn  by  lumbar 
puncture  in  a  case  which  recovered.  The  diplococci  wei'e  found 
within  the  cells.     Scherer^^®  investigated  an  epidemic  of  meningitis 


73 

in  an  array  corp  in  Stuttgart.  He  found  the  organisms  in  the 
meninges  in  two  eases  which  died,  and  in  the  nasal  secretion  in 
eighteen  cases.  He  thinlis  that  infection  of  the  nose  is  always 
present,  and  that  the  presence  of  the  diplococci  can  establish 
the  diagnosis. 

In  thirty-five  of  our  cases  on  which  post-mortem  examinations 
were  made,  diplococci  were  found  in  cultures  or  on  microscopic 
examination  of  the  exudation  or  in  sections  in  all  but  four  cases. 
In  most  of  the  cases  they  were  found  in  all  three  methods  of  exami- 
nation. In  one  case  in  which  they  were  not  found  they  had 
previously  been  found  in  the  fluid  withdrawn  by  spinal  puncture. 
Two  of  the  other  cases  were  chronic,  and  no  acute  lesions  were 
found.  The  fourth  case  was  a  chronic  case  with  a  mixed  infection 
with  tuberculosis.  The  diagnosis  of  the  mixed  infection  in  this 
case  was  made  from  the  character  of  the  lesions  in  the  meningitis, 
and  from  the  extension  of  the  inflammatory  exudation  along  the 
nerves  without  any  evidence  of  tubercular  lesions,  although  old 
tubercles  were  found  in  the  meninges.  There  was  marked 
infiltration  of  the  Gasserian  ganglia. 

In  a  certain  number  of  cases  cultures  failed  to  give  the  organisms, 
although  they  were  abundantly  present  both  on  cover-slip  exami- 
nation and  in  sections.  As  showing  the  diflSculty  in  growing  the 
organisms  in  cultures  made  from  the  meninges  at  the  post-mortem 
examination,  ten  cultures  were  made  in  one  case  from  the  exudation 
on  the  brain  and  six  from  the  cord,  cover-slip  examinations  showing 
abundant  organisms  in  the  cells.  Only  two  of  the  cultures 
from  the  brain  and  one  from  the  cord  showed  a  growth,  a 
single  colony  being  found  on  each  tube.  In  ten  cultures  from 
the  brain  and  nine  from  the  cord  in  another  case,  but  two  tubes, 
one  from  the  brain  and  one  from  the  cord,  showed  a  growth. 
As  a  rule,  the  organisms  were  more  easily  obtained  in  cultures 
made  on  the  acute  cases  than  on  the  chronic.  In  a  few  of  the 
cases  the  tubes  showed  a  very  abundant  growth  of  the  organisms, 
so  abundant  that  on  casual  inspection  of  the  tube  it  might  have 
been  taken  for  a  growth  of  the  pneumococcus. 

The  diplococcus  intracellularis  of  Weichselbaum  has  the  fol- 
lowing  characteristics   when    grown    in    pure    culture.      It  is    a 


74 

micrococcus  of  about  the  same  size  as  the  ordinary  pathogenic 
micrococci,  and  appears  in  diplococcus  form  as  two  hemispheres 
separated  by  an  unstained  interval.  It  stains  with  any  of  the 
ordinary  stains  for  bacteria,  and  is  decolorized  by  the  Gram 
method  of  staining.  There  is  considerable  irregularity  in  stain- 
ing, some  organisms  being  brightly  stained,  others  more  faintly. 
Sometimes  this  difference  in  staining  is  seen  in  a  single  pair  of 
organisms,  one  being  more  brightly  stained  than  the  other. 
There  may  also  be  considerable  variation  in  size,  and  the  larger 
organisms  stain  imperfectly.  In  the  swollen"  organisms  there 
is  often  a  brightly  stained  point  in  the  centre,  while  the  re- 
mainder of  the  cell  is  scarcely  colored.  It  may  have  been  this 
condition  which  was  mistaken  by  Jager  for  a  capsule.  These 
variations  in  size  and  in  staining  appear  to  be  due  to  degen- 
eration, and  are  more  common  in  old  than  in  fresh  cultures. 

The  two  organisms  are  usually  sharply  separated,  but  in  some 
there  seems  to  be  a  small  amount  of  material  uniting  them. 
Division  talies  place  usually  in  one  plane  giving  rise  to  diplo- 
cocci ;  tetrads  are  occasionally  seen.  There  is  little  or  no 
tendency  to  growth  in  the  streptococcus  form,  although  short 
chains  of  four  to  six  organisms  may  be  found.  We  have  never 
seen  the  streptococcus  formation  described  by  Jager,  and  in 
the  short  chains  the  longitudinal  line  on  which  he  lays  much 
stress  was  not  seen. 

In  cultures  the  organism  does  not  give  a  profuse  growth  on 
any  medium.  We  have  found  the  blood-serum  mixture  of  Loeff- 
ler  prepared  in  the  method  given  by  Mallory  the  best  adapted 
for  its  growth.  From  its  feeble  growth  on  agar  we  are  sure 
that  had  this  been  generally  used  for  the  first  cultures  the  or- 
ganism in  many  instances  would  not  have  been  found.  This 
is  particularly  the  case  when  other  organisms  are  present.  In 
all  cases  a  large  number  of  organisms  appear  to  be  dead, 
or  at  least  they  do  not  grow.  In  no  case  was  it  possible  to 
obtain  a  continuous  growth  over  the  surface.  Even  when  a 
large  quantity  of  an  exudation  which  on  microscopic  examina- 
tion contained  large  numbers  of  the  organisms  was  smeared 
over    the    surface,   only   single    colonies    would    develop.      The 


^o 


same  was  true  in  transplanting  colonies ;  in  the  place  of  a 
streak,  single  colonies  would  develop  in  the  line  of  the  needle. 
To  be  sure  of  obtaining  growth  it  was  necessary  to  make  a 
number  of  cultures,  using  large  amounts  of  the  material  investi- 
gated. To  keep  pure  cultures  going,  transfers  were  made  daily 
and  four  or  five  tubes  inoculated.  On  some  of  them  the  growth 
would  usually  fail. 

On  the  Loeffler  serum  mixture  the  growth  forms  round 
whitish,  shining,  viscid-looking  colonies,  with  smooth,  sharply 
defined  outlines,  and  may  attain  a  diameter  of  1  to  1^  mm.  in 
twenty-four  hours  (Plate  I.,  Fig.  1).  The  colonies  tend  to  be- 
come confluent,  and  do  not  liquefy  the  blood  serum.  In  acute 
cases,  when  large  numbers  of  the  organisms  are  present,  there 
is  in  some  cases  an  abundant  growth  of  minute,  round,  trans- 
parent colonies,  bearing  much  resemblance  to  the  pneumococcus 
lanceolatus  (Plate  I.,  Fig.  2).  There  is  a  better  growth  when 
the  serum  is  freshly  prepared. 

The  growth  is  feeble  on  plain  agar,  but  better  on  glycerine 
agar,  though  not  so  good  as  on  blood  serum.  On  glycerine 
agar  the  organism  forms  round,  pearly,  translucent,  flat,  shining, 
viscid-looking  colonies,  with  smooth,  sharply  defined  outlines. 
On  examination  with  low  power  they  are  homogeneous,  semi-trans- 
parent and  faintly  brownish,  with  transparent,  sharply  defined, 
smooth  margins.  They  rapidly  become  confluent.  On  agar  it 
is  often  impossible  to  obtain  a  second  growth. 

In  bouillon  the  growth  is  feeble  and  the  medium  becomes 
only  slightly  cloudy.  At  the  bottom  of  the  test  tube  there  is 
a  scanty  grayish-white  sediment,  which  rises  up  as  a  viscid 
string  when  the  tube  is  shaken.  On  potato  it  has  no  visible 
growth,  and  it  produces  no  change  in  litmus  milk. 

In  the  tissues  the  diplococcus  is  almost  strictly  confined  to 
the  interior  of  the  polynuclear  leucocytes  (Plate  III.,  Figs. 
1  and  2).  It  was  never  found  in  the  bodies  of  other  cells. 
In  the  cell  it  has  no  definite  position,  and  is  never  found  in  the 
nucleus.  When  smears  of  an  exudation  are  made,  appearances 
suggestive  of  this  may  be  found,  but  they  result  from  the  dis- 
tortion  of   the   cells    in    making    the    preparation.     In    paraffine 


76 

sections,  in  wliich  the  cells  are  better  shown,  nothing  similar  is 
seen.  The  numbers  found  in  the  cells  varied  from  a  single 
pair  in  a  cell  to  cells  so  packed  with  them  that  the  nucleus 
was  obscured.  The  greatest  numbers  were  found  in  the  leuco- 
cytes in  the  lungs  in  cases  of  diplococcus  pneumonia  (Plate  III., 
Fig.  2).  There  is  no  difficulty  in  demonstrating  their  presence 
in  the  tissues  when  the  method  of  hardening  and  staining 
recommended  is  used.  In  the  cells  the  same  irregularity  in 
size  and  in  staining  was  found  which  has  been  described  in 
the  pure  cultures. 

In  no  case  were  the  diplococci  found  except  in  connection 
with  the  lesions  of  the  disease.  So  far  as  could  be  learned 
from  cultures  of  blood,  liver,  spleen  and  kidneys  which  were 
made  at  each  post-mortem  examination,  it  never  produces  septi- 
caemia. It  is  possible  that  it  may  occasionally  have  been  pres- 
ent and  not  grown  on  the  cultures. 

Mixed  infections  with  other  organisms  were  not  uncommon. 
The  pneumocoecus  was  found  seven  times,  once  in  connection 
with  Friedlander's  bacillus.  Terminal  infections  with  staphy- 
lococci and  streptococci  were  occasionally  found. 

The  results  of  inoculation  show  that  the  organism  has  but  feeble 
pathogenic  powers  for  rabbits  and  guinea-pigs.  The  results  of 
our  inoculations  would  seem  to  show  a  still  more  feeble  patho- 
genesis than  has  been  obtained  by  previous  investigators.  All 
of  the  inoculations  made  in  the  subcutaneous  tissues  were  nega- 
tive. More  successful  results  were  obtained  from  inoculations 
into  the  peritoneum  and  pleural  cavities.  The  material  used  for 
inoculation  was  in  part  pure  twenty-four-hour  cultures  of  the 
organism,  in  part  the  fluid  containing  the  organisms  obtained 
from  lumbar  puncture,  and  in  part  portions  of  the  meningeal 
exudation  containing  the  organisms.  Inoculations  made  into 
the  spinal  canal  in  rabbits,  guinea-pigs  and  cats  in  all  cases  gave 
negative  results.  Out  of  a  large  number  of  inoculations  made 
into  the  peritoneal  and  pleural  cavities,  only  six  guinea-pigs  died. 
All  of  the  fatal  cases  were  inoculated  wilh  1  cubic  centimeter  of  a 
strong  bouillon  suspension  of  a  pure  culture  on  blood  serum 
twenty-four  hours   old.      Death  took   place   in  from  twenty-four 


77 

to  forty-eight  hours.  In  two  negative  cases  there  was  marked 
emaciation  of  the  animals,  but  there  were  no  lesions  found  on 
killing  them. 

In  the  successful  inoculations  in  the  pleural  and  peritoneal 
cavities,  inflammation  with  slight  fibrino-purulent  exudation  was 
found.  The  entire  peritoneum  was  injected,  there  was  a  small 
amount  of  fluid  present  in  the  cavity  and  a  slight  fibrinous  ex- 
udation over  the  surface  of  the  liver.  Microscopic  examination 
of  the  exudation  showed  pus  cells  which  contained  enormous 
quantities  of  the  organisms.  In  some  cases  a  cell  was  so  filled 
with  these  that  the  nucleus  could  not  be  made  out.  Among  the 
organisms  in  the  pus  cells  there  was  a  large  number  of  swollen 
and  degenerated  forms.  The  organisms  were  obtained  from  cult- 
ures from  the  peritoneal  cavity,  but  there  was  no  invasion  of  the 
tissues.     The  same  condition  was  found  in  the  pleural  cavity. 

The  only  successful  inoculation  resulting  in  the  production  of 
a  typical  meningitis  was  made  on  a  goat.  This  animal  was  in- 
oculated in  the  spinal  canal  with  1  cubic  centimeter  of  a  bouillon 
suspension  of  a  pure  culture  of  the  diplococcus  from  an  acute  case 
at  the  Massachusetts  General  Hospital.  The  inoculation  was  made 
in  the  afternoon,  and  the  animal  was  found  dead  the  next  morning 
at  ten  o'clock,  having  evidently  been  dead  for  several  hours. 

Macroscopically  nothing  could  be  made  out  beyond  intense  in- 
jection of  the  meninges  of  both  brain  and  cord,  with  slight 
cloudiness  in  the  meninges  of  the  brain  along  some  of  the  ves- 
sels and  a  slight  increase  in  the  meningeal  fluid.  Microscopically 
in  the  brain  there  was  deep  injection  of  the  blood  vessels  and  in 
the  meninges  an  exudation  composed  principally  of  pus  cells. 
There  was  very  little  fibrin  and  only  small  numbers  of  diplococci 
in  the  pus  cells.  The  purulent  infiltration  extended  from  the 
meninges  into  the  brain,  following  along  the  vessels,  and  in  the 
outer  layer  of  the  cortex  there  were  scattered  pus  cells  at  a  dis- 
tance from  the  vessels  (Plate  III.,  Fig.  3).  The  tissue  of  the 
meninges  was  swollen,  the  fibres  softened  and  separated,  the 
cells  were  swollen,  and  there  seemed  to  be  beginning  prolifera- 
tion, although  no  nuclear  figures  were  found.  No  change  could  be 
made  out  in  the  neuroglia.     In  the  cord  the  purulent  infiltration 


78 

of  the  meninges  was  not  so  marked  as  in  the  brain,  and  here  only 
pus  cells  were  found.  A  section  of  one  of  the  ganglia  of  the  cord 
showed  that  the  purulent  exudation  had  extended  up  to  this,  and 
a  few  pus  cells  were  found  among  the  ganglion  cells.  The  sec- 
tions stained  to  show  degeneration  showed  a  very  slight  but 
perfectly  obvious  degeneration  in  both  the  anterior  and  posterior 
nerve  roots.  In  the  tissues  of  the  cord  a  few  degenerated  and 
swollen  fibres  were  found. 

The  diplococcus  was  obtained  in  pure  culture  both  from  the 
brain  and  cord.  The  other  organs  were  sterile,  and  showed  no 
change  microscopically  beyond  slight  cloudy  swelling  of  the 
l^idneys. 

This  case  is  interesting  not  only  in  being  a  positive  inocula- 
tion, but  as  showing  how  extensive  a  pathological  condition  can 
be  produced  in  so  short  a  time.  An  inoculation  made  at  the  same 
time  in  the  spinal  canal  of  a  sheep  with  the  same  amount  of  the 
same  culture  was  negative. 

The  following  observations  were  made  on  the  viability  of  the 
organism :  — 

Oct.  1,  1897.  Cultures  (7)  made  from  a  fluid  which  had  been 
obtained  by  lumbar  i^uncture  and  had  been  kept  at  room  temperature 
for  eight  days,  were  sterile.  (This  fluid  had  shown  an  abundance  of 
organisms,  and  good  cultures  had  been  readily  obtained  from  it  pre- 
viously.) 

Sept.  30,  1897.  Cultures  on  blood  serum,  twenty-four  hours'  growth, 
were  dried  on  sterile  paper  in  sterile  Petri  dishes  and  placed  (1)  in  di- 
rect sun-light,  (2)  in  thermostat  at  37.5°,  and  (3)  dark  drawer,  room 
temperature,  for  twenty-four  hours  respectively.  Plants  then  were 
made  on  blood  serum  with  negative  result  in  Nos.  1  and  2,  but  positive 
in  3. 

Dried  preparations  in  dark  after  forty-eight  hours  and  sixty  hours 
produced  growth  when  planted  on  blood  serum;  after  seventy-two  and 
ninety-six  hours,  they  were  sterile. 

1.  Action  of  formaldehyde  gas,  on  smears  of  oi'ganisms  on  jDaper  in 
bell  jar,  exposed  for  four  to  seven  hours. 

Dilutions  of  1-7500, 1-15000, 1-30000, 1-60000,  1-20000, 1-225000  destroy 
vitality.    Plants  on  bouillon  and  blood  serum  sterile. 

Smears  of  organisms  on  j^aper  exposed  to  continuous  action  of  formal- 
dehyde for  eighteen  houi's,  in  rooms  of  1,200  and  9,000  cubic  feet  respec- 
tively, show  no  growth  Avhen  planted  on  blood  serum. 

2.  Bouillon  containing  carbolic  acid  in  proportion  of  1-100,  1-300, 
1-500,  1-600,  1-700  and  1-800  prevents  development  of  organisms. 


79 


LUMBAR   PUNCTURE. 

Lumbar  puncture  was  performed  in  fifty-five  cases,  and  in 
some  of  these  several  punctures  were  made.  Diplococci  were 
found  either  on  microscopic  examination  or  in  cultures  in  thirty- 
eight  cases.  In  seventeen  of  the  cases  they  were  absent.  The 
average  duration  of  time  from  the  onset  of  disease  before  spinal 
puncture  was  made  was  seven  days  in  the  positive  cases,  and 
seventeen  days  in  the  negative  cases.  The  longest  time  after 
onset  in  which  the  puncture  was  positive  was  twenty-nine  days. 
The  negative  cases  were  most  numerous  in  the  early  part 
of  the  epidemic,  before  we  had  realized  how  difficult  it  was  to 
obtain  cultures  of  the  diplococci  in  all  cases.  When  but  few 
organisms  were  present  they  could  easily  be  missed  on  micro- 
scopic examination,  and  even  when  present  in  large  numbers 
cultures  made  in  the  usual  way,  by  spreading  a  loop  full  of  the 
exudation  on  the  surface  of  the  medium,  frequently  showed  no 
growth.  How  difficult  it  was  in  some  cases  to  obtain  cultures 
is  seen  from  the  notes.  In  case  49,  in  which  cultures  were 
made  by  pouring  1  cubic  centimeter  of  the  fluid  obtained  over 
the  slanting  surface  of  the  culture  media,  on  one  tube  one 
colony  developed,  three  on  a  second  and  none  on  four  others. 
In  case  68,  fifteen  tubes  were  used.  On  two  of  the  tubes  there 
were  two,  and  on  one  ten  colonies  of  the  organisms.  In  this 
case  microscopic  examination  of  the  fluid  showed  considerable 
numbers  of  diplococci  and  pus  cells.  Toward  the  last  of  the 
epidemic  there  were  no  negative  results  when  the  spinal  punct- 
ure was  made  early  and  the  tubes  inoculated  with  a  large  amount 
of  material.  The  character  of  the  fluid  obtained  varied  greatly. 
In  some  cases,  even  when  diplococci  were  found  in  it,  it  was 
almost  clear,  showing  only  a  slight  turbidity  when  held  before 
a  dark  background.  In  most  of  the  cases  where  the  puncture 
was  made  early  in  the  disease  the  fluid  was  turbid,  in  some 
almost  like  pus,  and  in  twenty-four  hours  a  large  sediment 
formed  in  the  bottom  of  the  tube.  When  the  fluid  was  most 
turbid  there  was  little  or  no  formation  of  fibrin  ;  in  some  cases 
the  fluid  became  gelatinous  on  standing,  from  the  abundant  for- 


80 

mation  of  fibrin.  We  have  not  considered  those  cases  in  which 
no  fluid  was  found,  and  those  in  which  pure  blood  was  obtained. 

Interesting  results  were  obtained  in  those  cases  in  which  sev- 
eral spinal  punctures  were  made  during  the  course  of  the  dis- 
ease. In  these  cases  there  was  found  a  diminution  in  turbidity, 
often  accompanied  by  absence  of  organisms  in  fluids  withdrawn 
last.  In  one  chronic  case  three  punctures  were  made,  one  be- 
fore, one  after  and  one  during  an  exacerbation.  In  the  fluid 
obtained  before  and  after  the  exacerbation  no  diplococci  were 
found.  The  fluid  obtained  by  the  puncture  during  the  exacer- 
bation was  more  cloudy,  and  contained  diplococci.  Microscopic 
examination  of  the  fluid  agreed  perfectly  with  the  character  of 
the  lesions  in  the  meninges.  In  the  fluid  obtained  in  early 
punctures  two  to  three  days  after  the  onset  almost  the  only 
cellular  elements  were  polynuclear  leucocytes.  Later  the  large 
epithelioid  cells  of  the  meninges  were  found  among  the  pus  cells, 
often  enclosing  them.  A  small  number  of  lymphoid  cells  were 
found  in  many  cases,  and  were  numerous  in  the  chronic  cases. 
The  number  of  diplococci  found  on  microscopic  examination 
varied  greatly.  In  some  cases  they  were  so  numerous  that  in 
every  field  several  cells  containing  them  were  found ;  in  other 
cases  they  were  found  only  after  prolonged  search  for  them. 
They  were  occasionally  found  in  the  fluid,  their  presence  here 
being  probably  due  to  the  rupture  of  pus  cells  containing  them 
in  making  the  preparation.  They  were  only  found  in  the  poly- 
nuclear leucocytes.  "We  have  taken  the  following  description  of 
the  technique  of  the  operation  from  Wentworth's  description  in 
Mallory  and  Wright's  "  Pathological  Technique  "  :  — 

The  operation  and  the  subsequent  examination  of  the  fluid  should 
be  as  carefully  performed  as  any  other  bacteriological  investiga- 
tion, in  order  to  obtain  accurate  results.  The  back  of  the  patient 
and  the  operator's  hands  should  be  made  sterile.  The  needle 
should  be  boiled  for  ten  minutes.  The  patient  should  lie  on  the 
right  side,  with  the  knees  drawn  up,  and  with  the  uppermost 
shoulder  so  depressed  as  to  present  the  spinal  column  to  the 
operator.  This  position  permits  the  operator  to  thrust  the  needle 
directly  forward   rather  than  from  side   to   side.      An  antitoxin 


81 


needle,  4  cm.  in  length,  -with  a  diameter  of  1  mm.,  is  well 
adapted  for  infants  and  young  children.  A  longer  needle  is 
necessary  for  adults  and  children  over  ten  years  of  age. 

Aspiration  of  the  fluid  is  not  necessary,  but  some  operators 
prefer  to  attach  a  hypodermic  syringe  to  the  needle,  to  afford 
a  better  grasp  for  the  hand.  In  this  case  the  syringe  would 
have  to  be  detached  to  allow  the  fluid  to  flow.  The  additional 
manipulation,  and  possibly  the  defective  sterilization  of  the 
syringe,  might  impair  the  subsequent  bacteriological  examination. 

The  puncture  is  generally  made  between  the  third  and  the 
fourth  lumbar  vertebrae,  sometimes  between  the  second  and  third. 
The  thumb  of  the  left  hand  is  pressed  between  the  spinous  proc- 
esses, and  the  point  of  the  needle  is  entered  about  1  cm. 
to  the  right  of  the  median  line,  and  on  a  level  with  the  thumb 
nail,  and  directed  slightly  upward  and  inward  toward  the  median 
line.  Care  must  be  exercised  to  prevent  the  point  of  the  needle 
from  passing  to  the  left  of  the  median  line  and  striking  the 
bone.  At  a  depth  of  3  or  4  cm.  in  children  and  7  or  8  cm. 
in  adults  the  needle  enters  the  subarachnoid  space,  and  the 
fluid  flows  usually  by  drops.  If  the  point  of  the  needle  meets 
with  a  bony  obstruction,  it  is  advisable  to  withdraw  the  needle 
somewhat,  and  to  thrust  again,  directing  the  point  of  the  needle 
toward  the  median  line,  rather  than  to  make  lateral  movements, 
with  the  danger  of  breaking  the  needle  or  causing  a  haemorrhage. 
The  smallest  quantity  of  blood  obscures  the  macroscopic  appear- 
ance of  the  fluid  by  rendering  it  cloudy.  The  fluid  is  allowed 
to  drop  into  an  absolutely  clean  test-tube  which  previously  has 
been  sterilized  by  dry  heat  to  150°  C.  and  stoppered  with  cotton. 
The  fluid  should  be  allowed  to  drop  into  the  tube  without 
running  down  the  sides.  From  5  to  15  cubic  centimeters  of 
fluid  is  a  sufficient  quantity  for  examination." 

No  ill  effects  were  seen  from  spinal  punctures.  Dr.  Williams 
believes  that  the  withdrawal  of  the  exudation  may  be  of  positive 
benefit  to  the  patient.  A  note  in  one  case  says  the  patient 
became  very  much  quieter  and  slept  after  the  operation.  Too 
much  cannot  be  said  of  the  importance  of  the  procedure  in 
making  the  diagnosis  of  the  disease.     There  should  always  be  a 


82 

microscopical  and  bacteriological  examination  of  the  fluid  obtained, 
in  order  to  determine  what  organism  is  present.  If  the  puncture 
be  made  early  enough,  there  need  be  no  difficulty  in  distinguishing 
the  organisms  and  the  character  of  the  meningitis.  Acute 
meningitis  may.  be  due  to  a  variety  of  organisms  and  it  is 
important  to  know  which  is  present  for  this  has  an  influence  in 
making  the  prognosis,  and  in  the  future  it  may  be  of  importance 
in  influencing  the  treatment.  By  this  means  the  character  of 
the  meningitis  in  sporadic  cases  can  be  established,  for  there 
is  a  great  lack  of  definite  information  about  these  cases. 

PATHOLOGICAL  ANATOMY. 

In  the  literature  of  cerebro-spinal  meningitis  there  are 
numerous  accounts  of  post-mortem  examinations,  often  with  the 
details  of  the  microscopic  examination.  These  examinations 
have  been  made  both  in  acute  and  chronic  cases,  and  there  is 
considerable  uniformity  in  the  descriptions  of  the  lesions.  In 
many  cases  special  features  in  the  pathological  anatomy  have 
been  most  studied  and  a  general  application  of  the  results  of 
the  study  of  the  pathological  lesions  to  the  explanation  of 
symptoms  has  been  attempted.  The  descriptions  of  the  patho- 
logical changes  in  the  text-books  on  medicine  and  pathology, 
and  those  contained  in  the  special  treatises  on  the  disease  do 
not  seem  in  general  to  have  been  founded  on  personal  obser- 
vation, but  to  have  been  compiled  from  various  sources.  Most 
of  these  articles,  even  those  recently  published,  give  erroneous 
ideas  of  the  pathological  anatomy,  and  the  diplococcus  of 
"Weichselbaum  is  rarely  mentioned  in  connection  with  the 
pathogenesis.  Since  the  discovery  of  this  organism  there  has 
not  been  any  study  of  the  lesions  of  the  disease  in  their  con- 
nection with  the  organisms.  Certain  of  the  lesions,  especially 
those  connected  with  the  ear,  have  been  carefully  studied.  The 
study  of   the  eye  lesions  in  the  disease  have  not  been  so  good. 

"We  shall  make  no  attempt  to  give  the  entire  literature  of 
the  pathology  of  the  disease,  only  citing  the  most  important. 
Mathey"*  describes  a    yellow  gelatinous  exudation  in  the  mem- 


83 

branes  of  the  brain,  in  a  post-mortem  examination  made  on  one 
of  the  cases  of  Vieusseanx.  Danielson  and  Mann  made  post- 
mortem examinations  on  five  cases.  In  the  first  ease,  in  which 
the  symptoms  of  the  disease  were  of  twenty-two  hours'  dura- 
tion, they  found  only  hyperjemia  of  the  meninges.  In  another 
post-mortem  examination,  on  a  girl  in  the  same  family,  the 
disease  was  of  longer  duration,  and  they  found  a  fluid  resem- 
bling pus  between  the  pia  and  dura,  together  with  intense 
injection  of  the  vessels. 

The  committee  appointed  by  the  Massachusetts  Medical  Society 
in  1809^^  give  the  results  of  eight  post-mortem  examinations  in 
their  report.  The  lesions  they  found  differed  according  to  the 
duration  of  the  disease.  In  those  cases  dying  within  twelve 
hours  there  was  intense  congestion  of  the  membranes  of  the 
brain ;  in  the  cases  of  longer  duration  there  was  a  greenish 
yellow,  purulent  exudation.  The  ventricles  were  distended  and 
the  choroid  plexus  infiltrated.  In  one  case  there  was  acute 
pericarditis  and  pleurisy. 

The  lesions  were  more  carefully  studied  in  the  French  epi- 
demics from  1840  to  1845.  Rollet^'"''  thinks  that  both  from  a 
clinical  and  pathological  point  of  view  the  disease  can  be 
divided  into  two  categories.  In  one  of  these,  which  he  calls 
eerebro-spinal  meningitis,  the  lesions  are  confined  to  the  menin- 
ges. In  the  other,  which  he  calls  encephalo-meningitis,  there 
is  an  extension  into  the  substance  of  the  brain  and  cord. 
These  lesions  of  the  tissue  of  the  brain  and  cord  seem  to  have 
especially  engaged  the  attention  of  the  French  aiithors  at  this 
time.  They  were  recognized  by  Faure  Villar,^®'  who  describes 
both  general  and  localized  softening,  and  thinks  the  brain  is 
affected  in  all  cases  in  which  there  are  symptoms  affecting 
motion.  Chauffard^^^  says  he  has  recognized  alterations  of  the 
cord  consisting  of  foci  of  softening  containing  a  purulent  sub- 
stance, in  his  study  of  the  disease  in  Avignon.  He  was  so 
impressed  with  the  frequency  of  these  lesions  in  the  cord  that 
he  called  the  epidemic  in  Avignon  "  cerebro-spinite." 

Bohmer,^  who  investigated  an  epidemic  in  Cologne  in  1865, 
gives  a  very  good  description  of  the  pathological  anatomy.     He 


84 

describes  the  exudation  as  occurring  in  the  sub-arachnoid  space, 
and  most  abundant  over  the  base  of  the  brain.  The  ventricles 
were  only  slightly  dilated,  their  walls  were  soft  and  the  fluid 
in  them  increased  in  amount.  He  was  the  first  to  describe  the 
large  cells  in  the  exudation,  and  thinks  these  ai*e  the  mother 
cells  for  the  pus  cells  which  he  often  found  filling  them. 
He  found  the  same  large  cells  in  other  forms  of  meningitis 
than  the  epidemic,  but  they  were  then  filled  with  fat  instead  of 
with  young  cells.  In  some  cases  there  was  considerable  fibrin 
in  the  exudation.  In  the  substance  of  the  brain  and  cord 
there  was  serous  transudation  and  an  increased  number  of  cells 
in  the  perivascular  lymph  spaces,  as  well  as  small  collections  of 
cells  in  the  brain  itself.  He  never  found  enlargement  of  the 
spleen  or  any  change  in  the  intestinal  follicles. 

Klebs^*  investigated  the  pathological  lesions  in  the  epidemic 
in  Berlin  in  1865.  He  found  no  exudation  between  the  dura 
and  arachnoid.  He  attributed  the  large  amount  of  exudation 
found  at  the  base  of  the  brain  to  the  effect  of  gravity.  He 
found  softening  and  purulent  infiltration  in  the  tissue  of  the 
brain  and  fcord  and  in  some  cases  small  blood  extravasations  in 
the  white  matter.  Reichman^''^  thinks  there  is  a  difference  in  the 
pathological  lesions  between  epidemic  meningitis  and  the  other 
forms,  the  most  marked  difference  being  the  extensive  partici- 
pation of  the  meninges  of  the  cord  in  the  process  in  the 
epidemic  form. 

Probably  the  best  general  description  of  the  lesions  of  the 
disease  is  that  given  by  StrlimpeP^  He  found  purulent 
exudation  in  the  meninges  in  cases  which  macroscopically 
showed  no  abnormal  condition.  He  calls  special  attention  to 
tlie  participation  of  the  tissues  of  the  brain  and  cord  in  the 
process.  In  the  brain  a  small  zone  immediately  beneath  the 
meninges  is  infiltrated  with  round  cells,  and  these  foci  seem  to 
be  independent  of  the  vessels.  The  largest  of  the  areas  of 
cellular  infiltration  within  the  brain  are  around  the  vessels. 
There  is  marked  hypersemia  of  the  vessels  in  the  interior  of 
the  brain,  and  hsemorrhages  may  be  found.  There  are  histo- 
logical changes  in  the  nerves  of  both  brain  and  cord,  consisting 


85 

in  hypertrophy  of  the  axis  cylinders.  He  thinks  that  brain 
abscesses  may  arise  in  the  course  of  meningitis,  and  may  be 
the  result  of  a  meningitis  which  was  not  recognized.  He 
gives  the  history  of  three  cases  of  apparently  idiopathic  brain 
abscess   which   had   been   preceded   by   meningitis. 

Reichman  gives  an  account  of  the  lesions  in  a  chronic 
case  of  meningitis  which  lasted  from  the  5th  of  June  to  the 
14th  of  August.  The  pia  arachnoid  was  cloudy,  and  over 
the  base  of  the  brain  it  was  infiltrated  with  a  firm,  yellowish 
material.  The  same  infiltration  extended  through  the  foramen 
magnum  and  surrounded  the  cord  as  far  as  the  exit  of  the 
third  cervical  nerve.  The  convolutions  of  the  convexity  of 
the  brain  were  flattened,  the  ventricles  dilated.  The  brain 
substance  was  somewhat  oedematous  and  of  peculiar  elastic 
consistency.  The  pia  in  places  adhered  strongly  to  the  surface 
of  the  hemispheres,  portions  of  the  cortex  being  torn  off  in 
removing  it.  There  was  thickening  and  exudation  around  all 
of  the  cervical  nerves.  A  small  portion  of  the  cervical  cord 
appeared  to  be  softened. 

Meschede™  found,  in  a  post-mortem  examination  on  a  chronic 
case  of  meningitis,  characterized  by  marked  remissions  in  the 
course  of  the  disease,  partly  cicatricial  thickening  and  partly 
exudation   in   the    meninges   with   transitions   between   these. 

ClozeP  reports  the  examination  of  two  chronic  cases  of 
meningitis,  one  lasting  two  and  the  other  three  months.  No 
inflammatory  exudation  was  found,  but  there  was  considerable 
thickening  of  the  meninges  with  dilatation  of  the  lateral  ventricles. 

In  the  six  cases  of  meningitis  reported  by  "Weichselbaum,  in 
which  he  found  the  diplococcus  intracellularis,  there  was  an  acute 
exudation  in  the  meninges  of  the  brain  and  cord. 

Hagelstaram^"'^  investigated  the  histological  changes  in  the  spinal 
cord  in  eleven  cases  of  epidemic  cerebro-spinal  meningitis  in  Hel- 
singford.  He  found  the  changes  most  common  at  the  edge  of  the 
cord  about  the  blood  vessels  coming  from  the  pia.  In  this  part 
of  the  cord  there  was  small  cell  infiltration  and  various  degrees  of 
degeneration  of  the  nerves.  In  the  central  part  of  the  cord  there 
was  degeneration  in  the  nerve  fibres,  though  of  slighter  degree. 


86 


TABLE   OF   POST-MORTEM   EXAMINATIONS. 


Num-     Sex       Duration 
berof     and   ;  of 

Case.    Age.  i    Sickness. 


Condition  of 
Body. 


Brain. 


Cord. 


F.  14 


M.40 


M.40 


M.49 


M.22 


il.25 


P.  17 


F.  15 


7  days, 


26  days, 


7  days, 


14  days. 


Unknown, 
found  nn- 
conscions. 


2  days, 


5  days, 


5  days,    . 


Well  nourished,  1  Weight,  1,095  grams.     Overentire  Slight     exudation, 

abundant     adi-       surface  of  pia,  over  both  lateral  most   marked  on 

pose,     muscles!     convexiiies,  thin  purulent  exuda-  posterior  surface, 
pale.                     I     tion  and  cloudiness. 


Skin     pale,    ab-  j  Brain  bulging,  convolutions  flat-  Abundant    exuda- 

doraen  sunken,       tened.     Over  base  and   cerebel-  tlon  of  same  char 

muscles     thin       lum,  extending  up  over  convexi-  acter  as  in  brain, 

and  pale.                 ties,    a    dense     fibrino-purulent  particularly 

exudation.   This  extended  down-  marked  on  poste- 

wards,  filling  the  foramen  mag-  rior     surface     of 

num.    Lateral  ventricals  dilated,  i  dorsal  cord. 
The  ependyma  softened.     Exu-  I 
dation  in  fourth  ventrical. 

Good    muscular  '  Thick  fibrino-purulent  exudation    Exudation  of  same 
development.      over  base;  on  upper  surface  ex-       character  on  pos- 


Over  abdomen 
small  hyper- 
aemic  areas. 
Decubitus  over 
sacrum. 


Good    nutrition, 
pale. 


Blight  icterus, 


tends  over  frontal  lobes. 


terior  surface. 


Good    nutrition, 
rigor  mortis. 


Post-mortem  de- 
compo  sit  ion 
over  abdomen. 


Well  nourished, 
marked  rigor 
mortis. 


Softening  in  left  side  of  brain  in-    Exudation  along 
volving  fissure  of  Rolando.   Over       en  tire  posterior 
the  base,  extensive  exudation,  in-  i     surface, 
volving  cranial  nerves. 

Over   convexity  and   base   thick    Could  not   be  ex- 
fibrino-purulent  exudation.  amined. 


Very  slight  exudation  over  convex- '  Could    not    be    ex- 
ity  occurring  as  faint  yellowish        amined. 
streaks  and  cloudiness.    At  base  i 
and  in  ventricals  slight  amount 
of  cloudy  fluid. 


Tough  fibrino-purulent  exudation    Could    not    be    ex- 
over  base  extendingup  over  both        amined. 
lateral  convexities. 


Convexities  of  brain  showed  yel-  '  Exudation  abun- 
lowishexudationalongthecourse  '  dant  on  posterior 
of  vessels.  Slight  exudation  at  surface,  extend- 
base,  foci  of  softening  and  hem-  |  ing  around  nerves 
orrhage  in  white  matter.  j    of  cauda  equina. 


3  days,  .  Well  nourished.  Along  fissure  of  Sylvius  on  both  !  Slight  exudation 
sides  a  slight  yellowish  infiltra-  along  posterior 
tion  along  the  vessels;  at  the  surface  of  lumbar 
base  the  exudation  only  about  cord, 
optic  commissure. 


87 


TABLE   OF   POST-MORTEM   EXAMINATIONS. 


Heart. 

Lungs. 

Liver. 

Spleen. 

Kidneys. 

Cultures  and  Remarks. 

Myocardi- 
um rather 
Boft.slight 
a  r  t  e  r  i  0 
sclerosis. 

Slight  conges 
lion  and  oede- 
ma. 

Tissue 
opaque. 

Weight,  250 
grams;  on 
section    ho- 
mogeneous. 
Malpighian 
bodies  not 
visible. 

Weight,   360 
grams;  cap- 
sule   easily 
stripped, 
opaque  cor- 
tex, pale. 

Liver,  spleen   and   heart 
sterile.    Kidney  colon. 
Brain  cocci,  arranged  as 
diplococci.     Single  or- 
ganisms flattened. 

1 

Small,  nor- 
mal. 

Intense  conges- 
tion   posteri- 
orly in  both. 

Congested,   . 

No  rmal    i  n 
size  and  ap- 
pearan  ce; 
weight,  75 
grams. 

Congested,  . 

All  organs  sterile;  a  few 
diplococci    found    in 
sections. 

2 

Normal, 

Lower  lobe  of 
right    hyper- 
jemic,    with 
areas  of  bron- 
cho-pneumo- 
nia,  some   of 
which   coa- 
lesce. 

Pale,     . 

Rather    soft ; 
weight,    307 
grams. 

Pale,     . 

Lungs,   multiple    organ- 
isms,  chiefly  staphylo- 
cocci.    Brain  sterile, 
diplococci  found  on  sec- 
tions. 

3 

Normal,     . 

Foci   of    bron- 
cho-pneumo- 
nia in   lower 
lobes  of  both. 

Pale,     . 

Slightly    en- 
1  a  r  g  e  d  ; 
weight,    170 
grams. 

Normal, 

Pneumococci    in    lungs, 
spleen,    kidney   and 
heart;    in   brain   diplo- 
cocci. 

4 

Weight, 
500  gram  8. 
Fatty   de- 
generation 
of  myo- 
cardium. 
Slight   ar- 
terio-scle- 
rosis. 

Beginning  red 
pneumonic 
consolidation 
upper  lobe  of 
left,  lower  of 
right. 

Soft,  pale,    . 

Soft,    large, 
adherent  j 
weight,    300 
grams. 

Pale,     .        . 

Pneumococci    in    lungs. 
Heart,  liver,  sterile. 
Brain,  diplococci. 

5 

Slightacute 
pericardi- 
tis, ecchy- 
moses    in 
per  icar- 
dium. 

Congestion, 

Pale,     . 

Enlarged, 
soft;  weight, 
302  grams. 

Enl  arged ; 
hyperaemic 
ecchymoses 
in    cortex; 
markings 
obscure. 

In  brain   diplococci; 
other  organs  sterile. 

6 

Myocardi- 
um soft. 

Broncho  pneu- 
monia of  both. 
Lax  pneumo- 
nialowerlobe 
of  right. 

Pale,  cloudy. 

Slightly     en- 
larged   and 
soft;  weight, 
135  grams. 

Pale;  opaque, 

Lungs,  abundant  staphy- 
1 0  c  0  c  c  i ,  few  strepto- 
cocci.     Liver,    strepto- 
cocci ;  brain,  diplococci. 

7 

Normal,     . 

Muco-pus    in 
bronchi. 

Rather 
opaquewith 
some  injec- 
tion in  cen- 
tres of  lob- 
ules. 

Somewhat  en- 
larged; paler 
foUicles  dis- 
tinct; weight, 
195  grams. 

Normal, 

Liver,  spleen    and    kid- 
neys sterile.    Brain  and 
cord,  profuse  growth  of 
diplococcus.      Colonies 
of     streptococci    also 
found.    Only  diplococci 
found  in  sections. 

8 

Normal,     . 

Oongestion 
and  oedema  in 
lower  lobes. 

Moderately 
congested. 

Enlarged  ; 
weight,  215; 
follicles  nu- 
merous. 

Injected ; 
cloudy. 

Heart,  liver,  kidney  and 
b  rain  sterile.     Abun- 
dant   diplococci    found 
in  sections. 

9 

88 


TaUe  of  Post-mortem  Examinations —  Continued. 


Num- 
berof 
Case. 

Sex 
aud 
Age. 

43 

M.IQ 

44 

M.50 

S3 

M.27 

53 

M.24 

56 

F.  3| 

57 

M.24 

79 

M.oS 

59 

M.29 

66 

F.  28 

71 

M.   2 

Duration 

of 
SickncBB. 


Condition  of 
Body. 


Cord. 


3  days, 


5  days, 


2  days. 


9  days, 


5  days. 


2  days, 


30  days. 


6  days. 


6  days,    . 


29  days, 


Well  nourished, 
rigor  mortis. 


Well  nourished, 
good  muscular 
development. 


Well  nourished, 
rigor. 


Well  nourished. 
Herpes  about 
mouth  and  chin. 


Well  nourished. 


Well  nourished, 
slight  rigor. 


Good  muscular 
developmen  t, 
spare. 


Well  nourished. 


Well  nourished ; 
over  various 
parts  of  the 
body  h  e  m  or- 
rhages,  some 
■with  whitish 
centres. 


Great   emacia- 
tion. 


Vessels  of  meninges  deeply  in- 
jected. Faint  yellowish  streaks 
along  vessels  and  yellowish 
cloudy  fluid  in  meshes.  In  white 
substance  of  both  frontal  lobes 
ill-defined,  grayish,  softened 
areas.  Ecchymoses  in  white 
matter  generally. 


Abundant  gelatinous  fibrino-pur- 
ulent  exudation,  more  abundant 
on  right  side  and  over  base.  All 
the  cranial  nerves  involved  in 
the  exudation. 


Pi  a  over  convexity  and  base  infil- 
trated with  yellowish  exudation. 
In  ventricals  slight  exudation 
with  fibrinous  flocculi. 


Over  convexity  faint  yellowish 
exudation  along  blood  vessels. 
Over  the  base  an  abundant  fi- 
brino-purulent  exudation;  ven- 
tricals dilated,  contain  exudation. 
Exudation  along  cranial  nerves. 

Extensive  exudation  over  base, 
less  over  cortex.  Small  ecchy- 
mosis  in  corpus  striatum  and 
optic  thalamus.  In  white  sub- 
stance ecchymoses. 

A  slight,  grayish-yellow  exudation 
over  the  convexities,  along  blood 
vessels  and  in  the  sulci.  Slight 
over  base;  more  cloudiness  than 
visible  exudation. 

Thickening  of  pia  over  convexity, 
with  small,  opaque  yellowish 
foci  in  the  meshes.  Fibrinous 
and  in  part  organized  exudation 
over  base  and  in  ventricals,  in- 
duration of  brain. 


Similar   exudation 
in  cord. 


Could  not.be  examined, 


Great  amount  of  exudation  over 
entire  surface  of  brain,  particu- 
larly over  base.  Injection  of  ves- 
sels, exudation  in  ventricals, 
softening  of  ependyma.  Exuda- 
tion around  cranial  nerves. 


Pia  thickened,  cloudy;  yellow  foci 
in  meshes;  thick  exudation  at 
base  and  over  cerebellum.  Optic 
commissure  covered  by  thick  ex- 
udation. 


Similar  exudation 
in  cord,  involving 
all  the  nerves  of 
the  Cauda  equina. 


Exudation  well 
marked  along 
posterior  surface 
of  cord. 


Abundant    exuda- 
tion along  cord. 


Abundant    exuda- 
tion along  cord. 


Very  slight  exuda- 
tion along  cord 
posteriorly  and 
general  clo  ud  i- 
ness. 

Thickening  of 
meninges  of  cord. 


Abundant  exuda- 
tion along  cord, 
greatest  amount 
in  lumbar  region. 


Exudation  along 
entire  cord,  par- 
ticularly poste- 
rior surface. 


Thickening  of  me- 
ninges; accumu- 
lations of  thick, 
yellowish  masses 
posteriorly. 


89 


Table  of  Post-mortem  Examinations  —  Continued. 


Heart. 

Lungs.                 Liver. 

Spleen. 

Kidneys. 

Cultures  and  Remarks. 

Xormal,     . 

In   lower   lobe    Cloudy, 

Normal; 

Cloudy;  pale. 

Cultures  from  lung  and 

1 

of  right  lung 

weight,    120 

brain  diplococci.     Dip- 

i  1 1-d  e  ti  n  e  d 

grams. 

lococci   on    sections   of 

areas  of  con- 

lung  and  brain. 

solidatiou, 

size  of  pea  to 

that  of  bean. 

Diplococcus 

pneumonia. 

Normal,     . 

Ecchymoses    Normal, 

Soft;  weight. 

Cortex; 

Heart,   spleen,  liver  and 

2 

over  pleura. 

75  grams. 

cloudy. 

kidneys  sterile.    Diplo- 

Congestion , 

cocci  in  cultures  from 

posteriorly. 

cord. 

B  r  0  n  c  h  o 

pneumonia. 

Bronchiecta- 

tic  cavities. 

Normal, 

Hyperaemic,    . 

Pale,     . 

No  r  m  a  1 ; 
weight,    120 

grams. 

Normal, 

All  cultures  from  brain 
show    pure    diplococci. 
Mixture  of  other  organ- 
isms in  cord.     All  the 
other  organs  sterile. 

3 

Very  slight 

Fibrous  thick- 

Smallcentres 

Weight,     150 

Injected, 

Cultures  from  brain  gave 

4 

fibrinous 

ening  at  api-      of  lobules 

grams.     On 

colon    and    other    con- 

exadation 

ces. 

injected. 

section,  soft 

taminating    organisms. 

over  peri- 

and   flabby; 

Cord  gave  on  four  tubes 

cardium. 

follicles  vis- 
ible. 

pure  cultures  of  diplo- 
coccus. 

Normal,     . 

Foci   of    con- 
solidation. 
Diplococcus 
pneumonia. 

Pale,     . 

Weight,  29 
grams;  nor- 
mal. 

Normal, 

In  brain  and  cord  pure 
cultures   of    the   diplo- 
coccus.    Diplococci  in 
lungs.      Cultures   from 
upper   nasal   cavity 
showed  diplococci. 

5 

Normal,     . 

Old    tubercu- 

Slightly en- 

Enlarged; 

Injected, 

Heart,  liver,  spleen  and 

6 

lous    nodule.      larged. 

firm  on  pren- 

kidney   all   sterile.     In 

Injection. 

sure;  weight, 
210  grams. 

brain   and   cord   a  few 
colonies  of  diplococcus. 

Normal, 

CEdematous,   .     Cloudy,  lob- 

Weight,    145 

Normal, 

All  cultures  negative  save 

7 

ules    indis- 

grams;  folli- 

a   few    streptococci   in 

tinct. 

cles  visible. 

liver    and     kidneys. 

Brain  and  cord  sterile. 

Evidently    old    case, — 

older  than  history  given. 

Normal,     . 

Foci  of  consol- 

Normal, 

Weight,  85 

Normal, 

Cultures  from  cord  show 

8 

idation    with 

grams;  firm. 

diplococci.     Lungs 

necrosis    and 

follicles  vis- 

abundant pneumococci 

breaking 

ible. 

and    other    organisms. 

down. 

Other  organs  sterile. 

Normal, 

Injected  oedem- 

Large   i  n - 

Enlarged; 

Rather  large. 

Lung     staphylococcus. 

9 

atous. 

jected    lob- 

weight,   410 

vessels    in- 

aureus and  pneumo- 

ules,  very 

grams;  folli- 

jected; nor- 

ooccus.    Liver,  spleen, 

distinct  cel- 

cles distinct. 

m  al  mark- 

kidney and  heart  ster- 

lular   intil- 

ings. 

ile.      Brain     and    cord 

t  ration 

diplococcus. 

iu    portal 

spaces. 

Normal,     . 

Congestion 

Firm    and 

Small, smooth, 

Large ;  pale ; 

In  this  case,  spinal  punct- 

10 

and   broncho 

congested. 

firm;  weight. 

cortex  swol- 

ure  at  Children's  Hos- 

pneumonia. 

25  grams. 

len;  con- 
tain ecchy 
moses. 

pital    gave    diplococci. 
Child  acquired  diphthe- 
ria with  acute  glomenlo 
nephritis.    Cultures  at 
autopsy  showed   diph- 
theria bacilli. 

90 


Table  of  Post-mortem  Examinations  —  Continued. 


Num- 
ber of 
Case. 


Sex 
and 
Age. 


Duration 

of 
Sickness. 


Condition  of 
Body. 


Brain. 


Cord. 


F.  10 


5  days, 


2  days,     . 


"Well  nourished. 


Muscular;  well 
nourished  ; 
rigor  mortis. 


M.25 


5  days. 


Fairly  well  nour- 
ished. 


M  37 


M.31 


11.52 


10  days, 


37  days, 


30  days, 


9  days. 


14  days. 


Well  nourished, 


Emaciated, 


Emaciated, 


Well  nourished, 


Well  nourished; 
marked  rigor. 


23  days, 


Well  nourished; 
marked  rigor. 


Abundant  exudation,  yellowish 
soft  sero-purulent  in  places; 
serous  over  lateral  convexities 
and  base.  Cranial  nerves  in- 
volved in  exudation. 

General  serous  exudation  beneath 
pla  with  lines  of  deep,  thick  yel- 
low exudation  along  vessels  at 
base ;  abundant  exudation  around 
nerves. 


Abundant  exudation  over  base 
and  cerebellum,  extending  over 
cortex;  exudation  along  nerves; 
exudation  in  ventricals. 


Not  examined. 


Pia  thickened ;  frontal  lobes  ad- 
herent; red  thrombus  in  basilar 
artery  with  softening  of  pons. 


Pia  thickened;   small  amount  of 
exudation  along  vessels. 


Yellowish  purulent  streaks  along 
vessels  over  lateral  convexities; 
exudation  at  base  not  abundant. 


Abundant  purulent  exudation  ex- 
tending along  cranial  nerves  at 
base;  exudation  in  ventricals. 


Pia  oedematous,  thickened;  small 
amount  of  exudation,  except  here 
and  there  in  masses;  most  abun- 
dant in  base. 


Posterior  surface 
of  cord  hidden  by 
the  abundant, 
thick,  yellowish 
exudation. 

Vessels  of  menin- 
ges deeply  in- 
jected, with  only 
slight  exudation 
posteriorly. 


Abundant    exuda- 
tion. 


Abundant  exuda- 
tion on  posterior 
surface  of  lower 
dorsal  and  lum- 
bar. 


Thickening  of  me- 
nin  ges ,  with 
slight  exudation. 


Cloudy  fluid  in 
canal;  slight  exu- 
dation, thicken- 
ing. 

Thick  exudation 
posteriorly. 


Thick  exudation, 
most  abundant  in 
dorsal  and  lum- 
bar. 


Thick  exudation 
over  posterior 
surface  of  cervi- 
cal and  dorsal. 


91 


Table  of  Post-mortem  Examinations  —  Continued. 


Heart. 

Lungs. 

Liver. 

Spleen. 

Kidneys. 

Cultures  and  Remarks. 

Normal,     . 

Old  fibrous  ad- 

Normal, 

Normal; 

Vessels    i  n  - 

Pure  cultures  from  brain 

1 

hesions. 

weight,  .55 
grams. 

jected  ;  cor- 
tex opaque. 

and  cord  of  diplococcus. 

X^ormal,     . 

Id   lower  lobe 

Large,  . 

Capsule 

Firm;  nor- 

CultTires of  brain  sterile. 

2 

of  left  lung  a 

wrin  k  led; 

mal    mark- 

Diplococci    found     on 

large  area  of 

follicles  visi- 

ings. 

cover  slips  and  sections 

conBolidation 

ble;  weight, 

of  brain  and  lungs. 

wilh    puru- 

175 grams. 

lent     infiltra- 

tion and  par- 

tial  breaking 

down.  Diplo- 

C0CCU8  pneu- 

monia. 

Normal,     . 

In  both  lungs 

Normal, 

Small;  weight, 

Cortex  more 

Cultures  from  brain  and 

3 

foci    of    con- 

95 grams. 

opaque; 

cord    pure    diplococci. 

solidation 

m  arkings 

Diplococci  found  in  lung 

from    1    mm. 

normal. 

with   other   organisms. 

to  3  cm.  in  di- 

Other organs  sterile. 

ameter,    red- 

dish-gray in 

color,     sur- 

rounded    b  y 

yellowish 

zone.    Diplo- 

coccus   pneu- 

monia. 

Normal,  J  . 

Complete  red- 

Congested, . 

Small;  weight. 

Opaque; 

Cultures  from  lung  show 

4 

dish  -  gray 

80  grams. 

pale;  mark- 

pneumococci;  no   cult- 

consolidation 

ings    nor- 

ures from  cord.     Micro- 

of lower  lobe; 

mal. 

scope  shows  diplococci 

acute    pleu- 

in cord  and  in  abscess 

risy  ;    partial 

in   seminal  vesicles,  in 

consolidation 

latter     with     pneumo- 

of upper  lobe. 

cocci. 

Normal,     . 

Congested, 

Normal, 

Small ;  weight, 
105  grams. 

Normal, 

No  diplococci  found  in 
cultures,  nor  on  micro- 
scopic     examination. 
Condition    one   of 
chronic  meningitis  with 
abscess  following. 

5 

Normal,     . 

CEdema,  . 

Normal, 

Small;  weight, 
90  grams. 

Normal, 

Cultures  from  brain,  few 
diplococci. 

6 

Normal,     . 

Congested, 

Normal, 

Small;  weight, 
102  grams. 

Normal, 

Autopsy    3    days    after 
death.     Cultures   over- 
grown   with    contami- 
nating organisms.   Dip- 

1 

1 

lococci  found  in  sections 

of  the  cord. 

Normal,     . 

Foci  of  consol- 
idation ;    yel- 
1  0  wi  sh  cen- 
tres with  hy- 
peraemic    pe- 
riphery up  to 
3  cm.  in  diam- 
ter.    D  i  p  1  0  - 
coccus  pneu- 
monia. 

Normal, 

Slightly    en- 
larged; firm; 
weight,    170 
grams. 

Congested,  . 

Brain,  10  cultures,  2  show 
each  1  colony  of  diplo- 
coccus.    Cord,    6    cult- 
ures, 1  shows  1  colony 
of  diplococcus.    Lung, 
diplococcus,       strepto- 
coccus,   pneumococcus 
and      staphylococcus; 
sections  only  diplococ- 
cus. 

8 

Normal,     . 

Intense    injec- 
tion with  foci 
of  consolida- 
tion.    Biplo- 
coccus  pneu- 
monia. 

Normal, 

Soft;  follicles 
visible; 
weight,  85 
grams. 

Normal, 

Brain,  10  cultures,  1  tube 
shows  2  colonies  of  dip- 
lococci.    Cord,  9  cult- 
ures,  1    tube   shows  1 
colony   of  diplococcus. 
Heart,  liver,  spleen  and 
kidneys  sterile.     Lung, 

9 

pneumococci  and  Fried- 

lander's  bacillus. 

92 


Table  of  Post-mortem  Examinations  —  Concluded. 


Num- '  Sex   j    Duration 
berof    and  of 

Case.    Age.     Sickness. 


Condition  of 
Body. 


Cord. 


110 


F.  3J 


M.35 


M.31 


F.  21 


m:.43 


M.32 


m:.25 


3  days, 


3  days, 


74  days,    . 


35  days. 


Unknown, 
estimated 
at  7  to  10 
days. 


26  days, 


Well  nourished,  1  Over  both  lateral  convexities  foci 
of  yellowiBh  purulent  exudation 
along  vessels;  abundant  exuda- 
tion at  base. 


Good     muscular 
development. 


Greatly     emaci- 
ated. 


Emaciated, 


Slight  muscular 
development; 
spare. 


Emaciated, 


Slight  muscular 
deve  lopment; 
poor  nutrition. 


Exudation  abundant;  intense  hy- 
persemia  of  brain;  foci  of  hem- 
orrhage in  white  matter;  abun- 
dant exudation  at  base  along 
nerves. 


Firm,  organized  exudation  at  base : 
thickening  of  meninges;  small 
opaque  foci  in  meninges. 


Entire  pia  cloudy  and  thickened; 
over  base  firm  yellowish  exuda- 
tion with  more  opaque  foci. 

Over  entire  anterior  surface  of 
brain,  extending  down  over  lat- 
eral surfaces  and  over  occipital 
lobe  on  left  side,  abundant  yel- 
lowish, gelatinous  exudation; 
large  amount  over  base  and  cere- 
bellum. 

There  are  tubercles  along  vessels 
in  Sylvian  fissure  and  elsewhere ; 
tubercles  old  and  caseous.  Fi- 
brino-purulent  exudation  over 
base  with  few  tubercles;  puru- 
lent exudation  along  cranial 
nerves,  extending  to  gasserian 
ganglion,  which  was  infiltrated 
with  pus  and  granulation  tissue. 


Firm,  yellowish  exudation  along 
vessels  of  convexity,  best  marked 
laterally ;  abundant  exudation  at 
base. 


Cervical  cord  free; 
abundant  exuda- 
tion over  lower 
dorsal  and  lum- 
bar. 

Along  posterior 
cord ;  bestmarked 
in  lumbar  and 
dorsal;  ganglia 
swollen. 


Thickening  of  me- 
n  in  ges  ,  with 
opaque  foci. 


Firm  exudation 
along  posterior 
surface. 

Not  examined. 


Pia  of  cord  cloudy 
and  oedemntous; 
slight  exudation; 
no  tubercles. 


Not  examined. 


93 


Table  of  Post-mortem  Examinations  —  Concluded. 


Heart. 

Lungs. 

Liver. 

Spleen. 

Kidneys. 

Cultures  and  Remarks. 

Normal,     . 

Congestion  and 

Normal, 

Small;  weight. 

Normal, 

Cultures  from  brain  and 

1 

asdema. 

50  grams. 

cord     show     abundant 
pure  cultures  of  diplo- 
cocci. 

Normal,     . 

Large   area   of 

Normal, 

Slightly    e  n  - 

Fale,     . 

Five  cultures  from  lung 

2 

consolida- 

larged; firm ; 

all    show    abundant 

tion  ;   cedema 

weight,    200 

growth  of  diplococcus. 

and    hemor- 

grams. 

Diplococci   in   cultures 

rhage   at   pe- 

from brain  and  cord. 

riphery,  with 

confluent 

areas  of  puru- 

lent    iutiltra- 

tion.      Diplo- 

coccus   pueu- 

monia. 

Normal,     . 

Foci  of  consol- 

Firm,lobules 

Normal; 

Congestion 

No  cultures  made.  Spinal 

3 

idation     with 

prominent; 

w  e  i  g  h  t ,  60 

of    pyra- 

puncture April  8  gave 

softened  cen- 

increase  of 

grams. 

mids. 

diplococci.    Large  num- 

tres.     Diplo- 

connective 

bers  of  diplococci  found 

coccus  pneu- 

tissue and 

in    sections    of    lungs; 

monia. 

foci    of    in- 
fi  1 1  r  a  t  i  0  n 
around  por- 
tal spaces. 

none  found  in  sections 
of  brain  and  cord. 

Normal,     . 

Congestion 

Normal, 

Normal; 

Normal, 

Diplococci  found  in  cult- 

4 

and  broncho- 

weight, 70 

ures  and  in  sections  of 

pneumonia. 

grams. 

brain  and  cord. 

Normal,     . 

Congestion 

Normal, 

Firm;  slight- 

Normal, 

Cultures  and  cover  slips 

5 

and  oedema. 

ly  enlarged; 
weight,    130 
grams. 

from  brain  showed  pure 
diplococci.      Other   or- 
gans not  examined. 
Diplococci  found  in  sec- 
tions. 

Normal, 

Conglomerate 

Pew   tuber- 

Small; weight, 

Congested,  . 

From  lungs  pneuraococ- 

6 

tubercles  and 

cles  present. 

65  grams. 

cus;  cultures  of  brain 

tuberculous 

sterile.     This  case  was 

broncho-pneu- 

considered one  of  mixed 

monia. 

infection  of  meningitis 
with   tuberculosis.     In 
considering  it  epidemic 
meningitis,   the    main 
points  were  the  charac- 
ter of  the  exudation  and 
the  infiltration  extend- 
ing along  the  nerves. 

Normal,     . 

Congested, 

Congested,  . 

Normal; 
weight,  85 
grams. 

Congested,  . 

The  body  had  been  kept 
5  days  before  autopsy. 
Cultures   were  unsntls- 
factory,  being  over- 
grown with  various  or- 
ganisms.     Diplococci 
found   in   pus   cells    in 
the  ventricals. 

7 

94 

Flexner  and  Barker,  in  two  cases  investigated  by  them  in  the 
epidemic  in  Lanaconing,  Md.,  described  the  large  cells  in  the  men- 
inges and  small  foci  of  cellular-infiltration  in  the  brain  and  cord. 

When  we  review  these  brief  extracts,  we  find  that  in  the  most 
acute  cases  there  is  found  intense  hypersemic  of  the  meninges, 
with  purulent  infiltration  visible  only  on  microscopic  examination. 
In  cases  of  longer  duration  fibrino-purulent  exudation  is  present 
most  abundantly  over  the  base.  In  chronic  cases  fibrous  thicken- 
ing of  the  meninges  is  found  with  or  without  exudation.  The 
exudation  contains  pus  cells,  fibrin  and  large  cells  of  unknown 
origin.  Changes  in  the  tissue  of  the  brain  and  cord,  consisting 
of  cellular  infiltration,  of  abscesses  or  foci,  of  softening,  have 
been  described. 

The  preceding  table  (pp.  86-93)  gives  the  results  of  thirty- 
five  post-mortem  examinations.  In  most  cases  the  examina- 
tions were  made  a  short  while  after  death.  When  the  period 
was  longer  most  of  the  bodies  had  been  kept  preceding  the  ex- 
amination in  a  room  cooled  by  a  freezing  process  to  32°  to  35°  F. 
We  have  made  post-mortem  examinations  on  bodies  which  have 
been  kept  at  this  temperature  four  days  and  found  the  tissues 
almost  perfectly  preserved  ;  the  nuclear  figures  showed  nearly  as 
well  as  in  fresh  tissues.  In  a  few  of  the  bodies  which  were  kept 
at  ordinary  temperatures  the  tissues  were  not  so  good  and  the 
cultures  unsatisfactory.  At  every  autopsy  where  it  was  possible 
cultures  were  made  from  the  brain,  cord,  heart,  lungs,  liver, 
kidneys  and  spleen.  For  general  histological  purposes  portions  of 
the  brain,  cord  and  other  organs  were  hardened  both  in  Zenker's 
fluid  and  in  alcohol.  For  the  study  of  degenerated  nerve  fibres 
small  pieces  of  nervous  tissues  were  hardened  in  Miiller's  fluid 
or  in  formaldehyde  followed  by  Miiller's  fluid,  before  staining  in 
Marchi's  solution.  For  the  fixation  of  ganglion  cells  strong 
alcohol  was  employed. 

For  the  study  of  the  distribution  of  the  diplococcus  and  of  the 
histological  changes  in  the  tissues  eosin  followed  by  Unna's  alka- 
line methylene  blue  solution  was  found  to  be  by  all  odds  the  most 
satisfactory  stain.  The  advantage  of  Unna's  solution,  which  is 
considerably  more  alkaline  than  Loeffler's,  is  that  it  stains  bacteria 


95 

and  nuclei  in  tissues  hardened  in  Zenker's  fluid,  which  gives  a 
much  more  perfect  fixation  of  tissue  elements  than  alcohol. 
Imbedding  in  paraffin  was  used  almost  exclusively.  The  corro- 
sive crystals  were  removed  from  the  sections  after  cutting,  not 
from  the  blocks  of  tissue,  so  as  to  avoid  prolonged  treatment 
with  iodine,  which  acts  injuriously. 

The  steps  in  staining  are  as  follows  :  — 

1.     Stain  paraffin  sections  in  a  five  per  cent,  to  saturated  aqueous  solu- 
tion of  eosin,  twenty  minutes  to  one  hour. 
2      Wash  oif  in  water. 

3.  Stain  in  Unna's  alkaline  methylent  blue  solution  (methylene  blue, 
1 ;  cai'bonate  of  potassium,  1 ;  water,  100) ,  one  part,  diluted  with  nine 
parts  of  water,  for  one  to  two  hours. 

4.  Wash  in  water. 

5.  Decolorize  in  ninety-six  per  cent  alcohol  followed  by  absolute 
alcohol,  until  the  tissue  is  well  differentiated. 

6.  Xylol. 

7.  Balsam. 

Bacteria  and  organisms  stain  a  sharp,  clear  blue  ;  red  blood 
globules,  protoplasm,  fibrin  and  intercellular  substance  stain  of 
varying  shades  of  pink  and  lilac. 

A  little  practice  is  required  before  good  results  can  always  be 
obtained.  It  is  important  not  to  carry  the  decolorization  with 
the  alcohol  too  far. 

Nissl's  stain  for  ganglion  cells  and  Marchi's  stain  for  fatty, 
degenerated  nerve  fibres  require  no  special  mention. 

In  the  cases  on  which  post-mortem  examinations  were  made 
the  duration  of  illness  varied  from  two  days  up  to  seventy-four 
days.  The  average  duration,  leaving  out  of  consideration  the 
very  chronic  case  of  seventy-four  days,  was  eleven  and  one-third 
days,  this  being  taken,  not  from  the  stay  of  the  patient  in  the 
hospital,  but  from  the  initial  symptoms  of  the  disease.  The 
duration  is  really  much  less  than  this  for  the  average  number 
of  cases,  being  greatly  increased  by  seven  cases,  which  were 
twenty-three,  thirty-two,  twenty-three,  thirty-seven,  twenty-nine, 
thirty  and  twenty-six  days  respectively.  Leaving  out  these,  and 
the  seventy-four-day  case,  the  average  duration  is  six  and  one- 
half   days.      This   can   be   taken   as   the    average   of    the   acute 


96 

cases,  while  twenty-eight  and  one-half  days  can  be  considered 
as  the  average  of  the  chronic  cases,  here  again  leaving  out  the 
exceptional  case  of  seventy-four  days. 

The  condition  of  the  body  varied  in  the  acute  and  chronic 
cases.  In  the  acute  cases  the  body  was  generally  well  nourished, 
and  in  some  there  was  an  abundant  development  of  adipose 
tissue.  The  chronic  cases  presented  an  almost  characteristic 
appearance  ;  the  body  was  greatly  emaciated,  the  skin  was  pale, 
the  abdomen  sunken,  the  muscles  thin  and  pale.  In  one  case 
of  unknown  duration  there  was  slight  icterus.  The  presence  or 
absence  of  rigor  mortis  was  not  always  noted.  When  it  was  noted 
it  was  generally  very  well  marked  in  the  acute  cases  and  in 
most  of  the  chronic.  In  one  case,  which  was  of  but  six  days' 
duration,  there  was  a  decubitus  over  sacrum.  Evidence  of  herpes 
and  other  skin  lesions  were  not  as  apparent  at  post-mortem 
examinations  as  they  were  during  life.  In  one  case  there  was  a 
perfectly  characteristic  hsemorrhagic  eruption  over  various  parts 
of  the  body.  There  are  few  observations  with  regard  to  the  con- 
dition of  the  muscles.     They  were  generally  pale  and  cloudy. 

Lesions  of  the  Nervous  System. 

Macroscopic  lesions. 
The  lesions  produced  by  the  disease  may  be  divided  into  those 
affecting  the  meninges,  those  affecting  the  tissues  of  the  brain 
and  cord,  and  those  affecting  the  nerves.  The  lesions  of  the 
meninges  vary  in  their  extent  and  character,  this  depending 
mainly  upon  the  differences  in  the  intensity  and  acuteness  of 
the  process.  The  pathological  process  consists  in  inflammation, 
with  purulent,  sero-purulent  and  fibrino-purulent  exudation. 
TJie  most  marked  lesions  are  found  at  the  base  of  the  brain, 
extending  from  the  optic  commissure  backwards  over  the  crura, 
the  pons,  and  medulla.  The  meninges  of  the  entire  brain 
are  rarely  affected ;  the  exudation  on  the  convexity  is  usually 
most  intense  on  the  lateral  surfaces,  extending  for  some 
distance  on  either  side  of  the  fissure  of  Rolando.  In  some 
cases    it    is    more   marked    in   other    parts   of    the    brain,    and 


97 

the  principal  exudation  may  be  found  over  the  parietal  or 
even  the  occipital  lobes.  There  is  usually  little  or  no  exudation 
in  the  meninges  along  the  longitudinal  fissure.  The  meninges 
of  the  cerebellum  are  always  involved ;  the  exudation  extends 
over  the  under,  but  especially  over  the  upper,  surfaces  of 
this.  Along  the  upper  rim  of  the  cerebellum  masses  of  it 
from  two  to  six  mm.  in  thickness  may  be  found.  Small 
masses  of  it  may  also  be  found  along  the  vessels  of  the 
choroid  plexus.  The  exudation  is  chiefly  found  in  the  sulci 
along  the  vessels.  Karely  a  wide-spread  exudation  is  found 
covering  large  areas  of  the  brain. 

In  the  most  acute  cases,  those  dying  in  a  few  days  after  the 
onset,  the  changes  are  not  so  marked  as  in  the  more  advanced 
cases.  We  have  not  had  any  post-mortem  examinations  on  fou- 
droyant  cases  dying  within  ten  to  twenty-four  hours  after  the 
onset.  In  the  most  acute  cases  there  is  very  little  exudation. 
The  blood  vessels  of  the  pia-arachnoid  are  intensely  injected  ; 
not  only  do  the  large  blood  vessels  appear  as  red  lines,  but 
the  entire  surface  of  the  brain  has  a  pinkish  hue,  due  to  the 
injection  of  the  smaller  vessels.  The  exudation  appears  in 
yellowish  lines  in  the  sulci  along  the  vessels,  and  in  some 
cases  there  is  little  more  than  cloudiness.  There  is  more  or 
less  oedema  of  the  entire  meninges,  in  addition  to  the  purulent 
exudation ;  they  strip  off  easily  from  the  surface,  and  a  con- 
siderable amount  of  fluid  runs  out.  In  these  more  acute 
cases  there  seems  to  be  but  a  small  amount  of  fibrin,  and 
the  exudation  may  easily  be  removed  with  a  needle  from  the 
meshes  of  the  meninges.  In  the  loose  tissue  of  the  meninges 
of  the  base  of  the  brain  there  is  more  exudation,  and  it 
often  has  a  distinctly  purulent  character,  appearing  either 
diffusely  spread  over  the  surface  or  as  larger  or  smaller 
yellowish   masses. 

In  the  more  advanced  cases,  those  dying  from  five  to  twelve 
days  after  the  onset,  the  amount  of  exudation  is  much  greater 
and  it  contains  more  fibrin.  It  has  a  tough,  more  gelatinous 
character,  and  cannot  be  removed  from  the  meshes  of  the 
meninges   with   a   needle.     There   may   be    a   great    amount    of 


98 

it  at  the  base  of  the  brain  and  the  medulla  may  be  embedded 
in  it.  The  injection  is  marked,  but  not  so  intense  as  in  the 
more  acute  cases  (Plate  II.,  Fig.  1). 

In  the  chronic  cases  in  which  death  has  taken  place  in 
from  fifteen  to  thirty  days  from  the  acute  onset,  the  appear- 
ance of  the  meninges  differs  widely  from  that  in  the  acute 
(Plate  II.,  Fig.  3).  In  these  the  most  marked  condition  is 
the  oedema  and  general  thickening  of  the  meninges.  The 
change  is  most  marked  in  those  places  where  the  acute 
process  is  most  evident.  Along  the  vessels  the  meninges  are 
thickened  and  whitish ;  there  is  little  evident  exudation, 
yellowish  circumscribed  foci  scattered  here  and  there  in  the 
sulci  marking  the  remains  of  it.  The  meninges  at  the  base  are 
opaque,  enormously  thickened,  and  there  are  bands  of  organized 
tissue  extending  from  point  to  point.  In  one  of  the  most 
chronic  cases,  in  which  the  duration  of  the  disease  could  not 
be  ascertained  with  any  accuracy,  owing  to  the  mental  con- 
dition of  the  patient  when  he  was  brought  into  the  hospital, 
the  appearance  simulated  that  of  general  paralysis.  There 
was  marked  thickening  of  the  meninges  over  the  entire  frontal 
and  parietal  lobes  and  over  the  base  and  medulla.  The  only 
evidence  of  exudation  was  in  the  ventricles,  in  which  masses 
of  partly  organized  fibrin  were  found  adherent  to  the  walls. 
In  one  case,  the  duration  of  which,  from  the  imperfect 
history,  was  apparently  over  thirty  days,  in  addition  to  the 
thickening  of  the  meninges  the  entire  medulla  was  so  embedded 
in  a  dense  mass  of  connective  tissue  that  it  was  diflflcult 
to   remove   it. 

The  inflammation  is  confined  to  the  pia-arachnoid.  The  adjoin- 
ing surface  of  the  dura  is  smooth  and  there  is  little  injection  of 
the  vessels.  The  amount  of  fluid  in  the  subdural  space  is  in- 
creased in  amount,  and  it  is  more  cloudy  than  normal. 

The  process  in  the  meninges  of  the  cord  is  very  similar  to  that 
in  the  brain.  The  cord  is  always  affected  to  a  greater  or  less 
extent,  and  in  some  cases  the  lesions  in  the  cord  were  more 
marked  than  those  in  the  brain.  In  the  acute  cases  the  injec- 
tion of   the    inner  meninges  is  not  so  marked  as  in  the   brain, 


99 

but  there  is  intense  injection  of  the  dura.  The  amount  of  fluid 
in  the  sub-arachnoid  space  is  greatly  increased,  and  a  large 
amount  escapes  on  opening  this.  The  fluid  is  cloudy,  and  may 
contain  floculi  of  fibrin  and  pus.  The  exudation  is  always  most 
marked  along  the  posterior  surface  of  the  cord,  and  may  be  found 
here  in  large  amount,  while  the  anterior  surface  may  show  only 
cloudiness  and  injection.  All  parts  of  the  cord  are  not  affected 
to  the  same  degree  ;  there  is  usually  more  exudation  along  the 
dorsal  and  lumbar  cord  than  along  the  cervical,  though  the  re- 
verse of  this  was  often  found  (Plate  II.,  Fig.  2). 

In  the  chronic  cases  the  same  conditions  were  found  as  in  the 
brain.  There  was  general  thickening  of  the  meninges,  and  in 
the  place  of  a  general  and  diffuse  exudation,  there  were  scat- 
tered yellowish  patches  marking  the  remains  of  the  exudation. 

There  were  few  lesions  of  the  tissue  of  the  brain  and  cord 
apparent  to  the  naked  eye,  and  without  careful  microscopic  ex- 
amination lesions  which  must  be  regarded  as  among  the  most 
important  in  the  disease  would  have  been  over-looked.  All  these 
lesions  of  the  brain  and  cord  were  less  marked  in  the  most  acute 
cases.  The  ventricles  in  the  acute  cases  were  slightly  dilated  and 
the  fluid  increased  and  cloudy.  The  vessels  of  the  ependyma 
and  choroid  plexus  were  dilated.  In  the  posterior  cornua  of  the 
lateral  ventricles  there  was  usually  a  small  amount  either  of  pure 
pus  or  of  pus  and  fibrin.  In  more  advanced  cases  the  surface  of 
the  ventricles  had  lost  its  glistening  appearance  ;  it  was  softer  ; 
sometimes  almost  mushy  to  the  touch,  and  small  losses  of  sub- 
stance or  a  more  or  less  ragged  or  uneven  condition  of  the  surface 
were  found.  In  the  chronic  cases  the  dilatation  was  more  marked, 
the  surface  of  the  ependyma  uneven  and  covered  with  granula- 
tions. Section  of  the  brain  tissue  beneath  the  ependyma  showed 
this  to  be  looser  in  texture,  somewhat  more  transparent  and 
oedematous.  In  one  chronic  case  there  was  a  mass  of  connective 
tissue  and  organized  fibrin  which  completely  closed  the  foramen 
of  Magendie. 

In  the  acute  cases  the  meninges  stripped  off  easily  from  the  sur- 
face. In  one  chronic  case  they  were  adherent,  and  small  bits 
of  the  surface  of  the  brain  were  removed  on  stripping  them  off. 


100 

The  general  consistency  of  the  brain  is  little  altered ;  it  may 
be  somewhat  softer  to  the  touch,  owing  to  the  dilatation  of  the 
ventricles,  and  there  may  be  oedema.  The  vessels  both  of  the 
gray  and  white  matter  are  injected.  The  gray  matter  on  section 
may  have  a  pinkish  tinge,  and  blood  flows  from  the  sections  of 
the  dilated  vessels.  The  surface  may  be  softer,  and  punctiform 
hgemorrhages  may  be  found  in  it.  In  one  case,  which  was 
unfortunately  not  examined  microscopically,  there  was  distinct 
softening  over  a  considerable  area  of  the  lateral  surface.  In 
eight  cases  there  were  definite  macroscopic  lesions  in  the  tissue. 
These  consisted  for  the  most  part  in  haemorrhages,  in  the  white 
matter,  either  single  or  in  aggregations.  In  one  case  there  was 
an  area  of  distinct  softening  in  the  pons  adjoining  a  thrombus 
in  the  basilar  artery.  In  two  cases  there  was  hsemorrhage  with 
softening  of  the  cortex  of  the  cerebellum.  In  one  case  there 
were  foci  of  induration  in  the  basal  ganglia.  In  no  case  was 
there  definite  abscess  formation.  The  only  macroscopic  lesions 
noted  in  the  cord  were  increased  injection,  and  a  softer  consistency. 

The  cranial  nerves  were  affected  to  a  greater  or  less  degree 
in  all  cases.  The  nerves  most  affected  were  the  second,  the 
fifth  and  the  seventh  and  the  eighth.  The  nerves  were  embed- 
ded in  the  exudation  which  extended  along  them.  On  section 
they  were  swollen  and  reddened.  The  Gasserian  ganglia  were 
removed  in  a  number  of  cases,  and  in  all  they  were  found  swollen 
and  softened.  The  olfactory  bulbs  were  in  some  cases  slightly 
swollen.  The  exudation  could  often  be  followed  along  the 
seventh  and  eighth  nerves  into  their  foramina.  The  spinal 
nerves  were  also  affected.  The  nerve  roots  were  embedded  in 
the  exudation,  and  the  spinal  ganglia  red  and  swollen.  The 
exudation  around  the  nerves  was  often  particularly  prominent 
around  the  nerves  of  the  cauda  equina. 

In  two  cases  the  exudation  from  the  meninges  extended  into 
the  sella  tursica  aud  the  periphery  of  the  pituitary  body  was 
infiltrated  and  softened. 


101 


Microscopic  Lesions. 

The  results  of  the  microscopic  examination  of  the  tissues 
differ  according  to  the  aeuteness  of  the  process.  In  the  most 
acute  cases  in  which  there  was  but  little  change  on  macroscopic 
examination,  the  lesions  consist  in  purulent  infiltration  in  the 
meninges.  Even  in  the  advanced  cases  examination  of  the 
meninges  at  the  periphery  of  the  more  marked  lesions  shows 
purulent  infiltration  as  the  main  change.  The  blood  vessels  are 
injected  and  many  of  the  smaller  veins  contain  numbers  of 
leucocytes  both  within  the  vessels  and  infiltrating  the  walls.  The 
leucocytes  in  the  exudations  are  contained  in  the  tissue  in 
larger  and  smaller  masses,  the  largest  masses  being  in  the 
sulci.  In  the  meninges  over  the  surface  of  the  convolutions 
there  is  infiltration  of  the  tissue.  The  denser  tissue  on  the 
surface  (arachnoid)  is  infiltrated,  but  there  are  no  masses  of 
cells  in  this.  In  places  the  leucocytes  are  closely  packed 
together ;  in  others  they  are  found  scattered  in  a  finely  granular 
mass,  which  is  evidently  the  coagulated  albuminous  exudation. 
There  is  little  fibrin  among  the  cells.  The  leucocytes  are  exclu- 
sively the  polynuclear  variety,  the  nuclei  stain  intensely  and 
there  is  no  evidence  of  degeneration.  The  methods  used 
brought  out  very  distinctly  the  character  of  the  granulations  in 
the  leucocytes,  and  the  absence  of  eosinophilic  cells  was  remark- 
able. In  most  cases  not  a  single  eosinophile  cell  was  found. 
In  these  acute  cases  there  is  little  or  no  change  in  the  fixed 
cells  of  the  tissue.  Some  of  the  cells  of  the  walls  of  the  ves- 
sels  are  swollen,  but  there  is  no  evidence  of  proliferation. 

In  more  advanced  cases  the  number  of  cells  is  much  greater. 
They  appear  in  large  masses  in  the  meshes  of  the  tissue.  A 
part  of  the  mesh-work  evidently  represents  the  dilated  lymph 
spaces  of  the  tissue,  and  a  part,  in  which  the  meshes  are  much 
smaller,  represents  the  dilated  cell  spaces  of  the  more  compact 
tissue  of  the  surface.  In  some  cases  but  little  can  be  seen 
of  the  connective  tissue,  the  whole  tissue  being  infiltrated 
with  cells.  Here  also  the  cells  are  principally  polynuclear 
leucocytes  ;   in  most  of  them  the  nuclei  stain  brightly,  but  there 


102 

may  be  masses  of  them  in  the  middle  of  the  membrane  which 
are  swollen,  more  granular,  and  whose  nuclei  either  stain  im- 
perfectly or  not  at  all.  In  most  cases  there  are  no  red  cor- 
puscles in  the  exudation,  in  others  scattered  ones  may  be  found 
among  the  leucocytes,  and  in  one  case  areas  were  found  where 
the  exudation  had  an  almost  hsemorrhagic  character.  There  is 
more  fibrin  than  in  the  most  acute  cases.  It  appears  in  masses 
by  itself  or  as  a  delicate  net- work  among  the  pus  cells.  In 
one  case  there  was  a  considerable  amount  of  it,  and  in  places 
it  had  undergone  hyaline  metamorphosis.  It  is  never  present  to 
the  same  extent  as  it  is  in  other  forms  of  meningitis,  particu- 
larly that  produced  by  the  pneumococcus.  In  addition  to  the 
pus  cells  and  the  scattered  red  corpuscles  other  cells  appear  in 
the  exudation,  and  often  form  a  large  part  of  it.  These  are 
large  cells,  from  two  to  eight  times  the  diameter  of  a  leucocyte. 
They  are  present  to  some  extent  in  all  cases,  but  very  few  are 
found  in  the  most  acute  cases.  The  nuclei  of  these  cells  are 
large  and  vesicular,  the  protoplasm  stains  very  faintly  and  is 
finely  granular.  It  is  difficult  to  make  out  the  protoplasm  of 
the  largest  of  these  cells,  for  they  are  filled  with  other  cells 
which  they  have  taken  up  (Plate  VI.,  Fig.  2).  Polynuclear 
leucocytes,  often  in  considerable  numbers,  are  found  in  these 
cells.  In  one  as  many  as  fifteen  were  counted.  The  enclosed 
leucocytes  show  various  changes.  Most  often  they  are  contained 
in  a  vacuole  of  the  large  cell,  and  a  clear  space  can  be  seen 
around  the  periphery  of  the  enclosed  cell.  Rarely  lymphoid 
cells  may  be  found  in  them.  The  protoplasm  becomes  pale  and 
gradually  disappears,  while  the  nucleus  may  be  but  little  changed. 
Finally  the  nucleus  breaks  up  into  irregular  masses  of  chromatin, 
and  some  cells  are  found  which  are  filled  with  irregular  chromatin 
fragments.  The  large  vesicular  nucleus  of  the  cell  may  be  made 
out  lying  close  to  the  periphery.  In  most  cases  the  large  cells 
were  well  preserved,  in  others  they  were  among  masses  of  de- 
generating leucocytes,  and  seemed  to  undergo  the  same  degener. 
ation.  They  were  most  numerous  around  the  periphery  of  the 
cell  masses  of  the  exudation. 
These  large  cells   have   excited   the   interest  of   all  who  have 


103 

studied  the  process,  but  their  origin  has  been  obscure.  Owing 
to  the  freshness  and  variety  of  the  material  and  the  use  of 
improved  methods  of  technique,  it  has  been  possible  to  follow 
the  various  stages  of  their  formation.  In  the  place  of  the  few 
scattered  cells,  with  thin,  spindle-shaped  nuclei,  seen  in  the  con- 
nective tissue  of  the  normal  meninges,  the  nuclei  become  large 
and  vesicular,  and  the  protoplasm  of  the  cells  is  increased  in 
amount  and  granular.  These  cells  are  greatly  increased  in  num- 
ber, there  are  masses  of  them  around  the  blood  vessels  and 
in  the  connective  tissue.  The  spaces  in  the  tissue  enclosing 
the  pus  cells  may  be  lined  with  them.  Nuclear  figures  in  con- 
siderable numbers  and  in  great  variety  and  beauty  are  often 
seen  in  cells  which  are  still  in  connection  with  the  tissues,  and 
in  those  lying  free  among  the  cells  in  the  exudation.  By 
taking  different  cases,  and  sometimes  even  in  the  same  case, 
the  various  steps  in  the  formation  of  these  large  cells  from 
the  cells  of  the  connective  tissue  and  from  the  cells  lining 
the  lymph  spaces  in  the  tissue  could  be  followed.  The  con- 
nective tissue  fibres  become  less  evident,  and,  as  the  cells 
multiply,  they  become   swollen   or   disappear. 

The  vessels  are  dilated  and  in  some  of  them  thrombi  are  found. 
Masses  of  leucocytes  with  a  few  lymphoid  cells  among  them  are 
often  found  in  the  centre  of  the  vessels  among  the  red  corpuscles. 
Occasionally  a  few  lymphoid  and  plasma  cells  are  found  around 
the  vessels.  The  proliferative  changes  found  in  the  intima  of  the 
arteries,  which  are  so  common  in  tuberculosis  and  pneumococcus 
meningitis,  are  but  rarely  found  here.  This  change  consists  in  the 
loosening  of  the  endothelial  layer  of  the  intima,  and  the  forma- 
tion between  this  and  the  elastica  of  numbers  of  large  epithelioid 
cells,  which  appear  to  form  a  lining  to  the  vessel.  In  one  speci- 
men the  intima  of  a  small  artery  was  elevated  and  back  of  this 
was  a  clear  space  filled  with  polynuclear  leucocytes,  which  also 
to  some  extent  infiltrated  the  muscular  coat.  Some  degree  of 
purulent  infiltration  is  seen  in  wall  of  an  artery  (Plate  III.,  Fig.  2) 
which  is  from  a  case  of  experimental  meningitis  in  a  goat. 

In  the  chronic  cases  the  lesions  are  much  less  striking.  The 
exudation  is  confined  to  the  small,  yellowish  masses  mentioned 


104 

in  the  macroscopic  description.  These  are  composed  for  the 
most  part  of  masses  of  degenerated  pus  cells  and  nuclear  de- 
tritis.  At  the  periphery  of  the  masses  occasional  leucocytes  are 
seen  whose  nuclei  are  clearly  stained.  The  meninges  are  con- 
verted into  thick,  dense  masses  of  tissue,  resembling  cicatricial 
tissue,  which  contain  few  cells.  Here  and  there  in  the  tissue, 
especially  close  to  the  brain,  there  are  groups  of  cells.  In 
these  there  are  but  few  of  the  large  cells  which  form  such 
a  conspicuous  feature  in  the  acute  cases.  In  the  place  of  these 
we  find  in  the  cell  groups  and  around  the  vessels  numbers  of 
lymphoid  and  plasma  cells.  We  understand,  under  the  term 
plasma  cells,  cells  which  are  similar  to  those  described  under 
this  term  by  Unna.  They  have  a  nucleus  similar  in  its  general 
character  to  that  of  the  lymphoid  cell,  and  a  variable  amount 
of  granular  protoplasm  which  stains  blue  with  Unna's  alkaline 
methylene  blue  solution.  In  the  cell  groups  there  are  cells  which 
seem  to  show  transitions  between  the  lymphoid  and  plasma  cells. 
It  is  only  by  means  of  fine  sections  and  the  use  of  high  powers 
that  the  character  of  the  cells  forming  the  closely  packed  masses 
around  the  vessels  can  be  made  out. 

The  changes  in  the  meninges  of  the  cord  are  of  the  same 
general  character  as  those  of  the  meninges  of  the  brain.  The 
large  cells,  though  present,  are  not  so  numerous  as  in  the  latter. 
The  blood  vessels  are  injected.  The  greatest  mass  of  the  exu- 
dation is  invariably  in  the  meninges  on  the  posterior  surface  of 
the  cord.  The  pus  cells  lie  in  larger  masses  and  the  reticulum 
is  not  so  evident,  and  there  is  always  a  smaller  amount  of  fibrin 
than  in  the  meninges  of  the  brain.  In  cases  where  the  macro- 
scopic examination  showed  only  hypersemia  with  slight  cloudi- 
ness of  the  meninges,  as  on  the  anterior  surface  of  the  cord 
and  in  places  over  the  entire  surface,  microscopic  examination 
showed  well-marked  purulent  infiltration.  In  the  more  chronic 
cases,  just  as  in  the  meninges  of  the  brain,  the  purulent  exu- 
dation is  confined  to  small  areas  of  degenerated  pus  cells,  and 
there  is  thickening  of  the  meninges  with  cellular  accumulations 
around  the  vessels. 


105 


Lesions  of  the  Tissue  of  the  Brain  and  Cord. 
These  lesions  are  interesting  on  account  of  their  frequency, 
their  general  bearing  on  pathological  processes  and  from  being 
most  marked  in  the  particular  form  of  meningitis  which  is 
produced  by  the  diplococcus  intracellularis.  In  only  a  few  cases 
were  these  lesions  absent.  The  lesions  are  most  evident  in 
those  cases  in  which  from  five  to  ten  days  elapsed  from  the  onset 
of  the  disease  until  death.  The  blood  vessels  of  the  convexity 
are  injected,  the  cortex  in  most  cases  wider,  and  the  tissue  more 
loose  and  reticular,  as  though  cedematous.  The  lymph  spaces 
around  the  blood  vessels  are  dilated.  In  some  places  there  is 
a  circumscribed  infiltration  of  the  tissue  with  pus  cells  which 
extend  downward  from  the  infiltration  in  the  meninges.  The 
spaces  around  the  dilated  vessels  are  often  filled  with  pus  cells 
which  extend  from  here  into  the  surrounding  brain  tissue.  The 
infiltration  was  usually  most  marked  in  the  outermost  layer  of 
the  cortex  above  the  ganglion  cells,  but  in  some  cases  it  was 
found  deeper  down  among  the  ganglion  cells,  and  even  in  the 
white  matter.  In  addition  to  this  infiltration  around  the  vessels 
single  pus  cells  are  often  found  in  the  brain  tissue,  apparently 
remote  from  the  areas  of  infiltration.  There  were  but  few  haemor- 
rhages found  in  the  cortex  of  the  cerebrum.  In  two  cases  there 
was  extensive  softening,  with  purulent  infiltration  and  haemor- 
rhage in  the  cortex  of  the  cerebellum.  In  these  places,  which 
partly  extended  into  the  granular  layer,  the  cortex  was  repre- 
sented by  scattered  granular  masses,  among  the  pus  cells  and 
haemorrhage,  and  the  cells  of  Purkinje  had  disappeared,  or  only 
granular  fragments  of  them  were  found.  The  areas  in  the 
white  matter  which  showed  macroscopicaUy  as  hsemorrhages 
generally  appeared  as  foci,  composed  of  numerous  fine  hcemor- 
rhages,  with  but  little  infiltration  with  pus  cells.  Around  these  foci 
there  were  changes  in  the  neuroglia  which  will  be  presently 
described.  In  one  case  there  was  an  acute  focus  of  softening 
with  infiltration  with  pus  cells  in  the  pons  just  over  a  throm- 
bus in  the  basilar  artery.     In  this  area  the  tissue  was  distinctly 


106 

broken  down,  necrotic  and  infiltrated  with  pus  cells.  In  the 
most  chronic  case  there  was  a  firm  mass  resembling  a  gumma  on 
the  upper  surface  of  the  cerebellum  which  completely  closed  the 
foramen  of  Magendie.  On  microscopic  examination,  the  centre 
of  this  was  composed  of  totally  necrotic  pus  cells  and  fibrin,  with 
fine  remains  of  nuclear  detritis.  This  was  surrounded  by  a 
dense  mass  of  connective  tissue  with  infiltration  of  plasma 
cells  and  lymphoid  cells,  and  it  extended  downwards  through 
the  granular  layer.  It  seemed  to  have  resulted  from  the 
necrosis  of  a  large  purulent  exudation  in  the  meninges,  com- 
bined with  superficial  necrosis  of  the  tissue  of  the  cerebellum 
immediately  beneath.  In  several  of  the  chronic  cases,  in  which 
there  was  marked  thickening  with  cellular  infiltration  of  the 
meninges,  the  same  cellular  infiltration  was  found  around  the 
vessels  extending  into  the  tissue.  In  one  acute  case,  in  which 
almost  complete  paralysis  of  one  side  appeared  twenty-four 
hours  before  death,  the  exudation  was  most  marked  on  the  side 
of  the  brain  opposite  the  paralyzed  side.  In  this  place  the 
oedema  and  cellular  infiltration  of  the  cortex  was  most  marked. 
Macroscopically  the  cortex  was  much  swollen  and  softer.  Pus 
cells  were  found  not  only  in  large  numbers  around  the  vessels 
but  had  generally  infiltrated  the  brain  tissue.  At  various  places 
in  the  white  matter  and  in  the  internal  capsule  there  were 
small  foci  of   haemorrhage. 

In  no  case  in  which  the  ventricles  were  examined  were 
they  found  free  from  alteration.  The  ependymal  lining  was 
in  some  cases  preserved,  in  others  it  was  lost  over  greater 
or  smaller  areas.  The  tissue  beneath  the  ependyma  was 
loose,  reticular  and  oedematous.  The  blood  vessels  were  injected 
and  there  was  more  or  less  infiltration  with  pus  cells  both 
immediately  around  the  vessels  and  at  a  distance.  In  many 
of  the  chronic  cases  the  surfaces  of  both  the  lateral  and 
fourth  ventricles  were  covered  with  granulations. 
'  The  tissue  of  the  cord  was  always  less  affected  than  that 
of  the  brain.  Only  in  one  case  did  we  find  a  purulent 
infiltration  of  the  cortex  extending  from  the  meninges  with 
foci   of   infiltration   in   the   tissue. 


107 

The  most  interesting  changes  concern  the  neuroglia.  These 
were  found  both  in  the  cortex  and  beneath  the  ventricles, 
and  in  the  neighborhood  of  the  foci  of  softening.  With  a 
low  power  there  is  a  distinct  increase  in  the  cells  of  the 
cortex  outside  of  the  ganglion  cells,  which  is  both  general 
and  more  marked  in  certain  places.  With  high  power  the 
cells  of  the  neuroglia  are  swollen,  their  nuclei  are  large, 
clear,  vesicular,  and  contain  larger  and  smaller  masses  of 
chromatin.  Around  these  large  nuclei  there  is  a  faintly 
stained,  very  much  branched,  irregular  mass  of  granular 
protoplasm.  This  presents  some  similarity  to  a  branched 
connective  tissue  corpuscle,  but  can  be  distinguished  from  it 
by  the  more  faintly  stained  and  more  granular  character  of 
the  protoplasm.  The  shape  of  the  cells  varied ;  some  were 
branched  in  all  directions,  while  others  were  more  spindle- 
shaped,  with  short  secondary  protoplasmic  prolongations  from 
the  main  branches.  Many  of  the  cells  contained  two  nuclei, 
and  in  places  there  were  groups  of  four  or  more  nuclei 
closely  clustered  together  with  a  considerable  amount  of  proto- 
plasm around  them  (Plate  VII.,  Fig.  4).  In  all  these  places,  in 
favorable  tissues,  varying  numbers  of  nuclear  figures  were  found 
(Plate  VI.,  Figs.  2  and  3).  They  presented  the  same  forms 
as  other  multiplying  nuclei,  and  in  some  cases  the  spindles 
and  centresomes  were  distinct.  Apparently  for  the  recognition 
of  these  nuclear  figures  much  depends  either  upon  the  condition 
of  the  tissue  or  the  period  of  the  disease.  They  were  numerous 
in  one  specimen,  while  in  others,  in  which  there  was  evident 
proliferation,  they  could  be  found  only  after  prolonged  search. 
In  some  of  the  places  where  the  proliferation  was  most 
marked  there  was  some  infiltration  of  the  tissue  with  pus 
cells ;  in  others  the  nuclear  figures  were  found  at  a  distance 
from  such  infiltration  and  in  apparently  normal  tissues.  The 
same  change  in  the  neuroglia  was  found  deeper  down  in  the 
cortex  among  the  ganglion  cells.  The  number  of  nuclei 
around  the  ganglion  cells  was  increased,  and  in  several  instances 
nuclear  figures  were  found  in  these  places.  The  greatest  increase 
in  the  neuroglia  was  found  around  the  foci  of  haBmorrhage  and 


108 

cellular  infiltration  in  the  white  matter.  The  haemorrhagic  area 
was  often  surrounded  by  an  area  made  up  of  proliferating 
neuroglia  cells,  and  areas  composed  of  them  were  often  found 
apart  from  such  haemorrhages ;  but  these  seemed  probably  to  be 
the  peripheries  of  haemorrhages  which  did  not  appear  in  the 
section.  In  all  of  these  places  there  were  numerous  nuclear 
figures.  The  same  proliferation  in  the  neuroglia  with  the 
presence  of  nuclear  figures  was  also  found  in  the  acute  areas 
of  softening  in  the  cerebellum  and  in  the  neuroglia  of  the  optic 
and  olfactory  nerves. 

In  every  case  proliferative  changes  in  the  neuroglia  were  found 
in  the  tissue  of  the  ventricles.  Where  the  ependymal  lining 
was  preserved  the  cells  were  closely  packed  together,  the  nuclei 
were  large  and  proliferation  had  evidently  taken  place,  but  no 
definite  nuclear  figures  were  found.  Beneath  this  the  tissue 
was  loose  and  reticular,  and  contained  large  numbers  of  single 
cells  and  cell  groups.  The  first  nuclear  figures  were  found 
in  the  neuroglia  cells  here,  but  they  were  not  as  numerous  as 
in  the  cortex  and  in  the  white  matter.  In  the  more  chronic 
cases  the  changes  in  the  neuroglia  of  the  cortex  were  not  so 
marked  as  in  the  acute.  There  was  some  increase  in  the  cells, 
most  of  which  assumed  a  normal  appearance,  the  tissue  was 
denser  and  the  fibres  more  evident.  These  more  chronic  changes 
in  the  neuroglia  were  best  studied  in  the  ventricles.  In  these 
there  was  a  dense  lining  of  neuroglia  with  rather  coarse  fibres, 
and  with  a  greatly  increased  number  of  cells  immediately  beneath 
the  ependyma  and  extending  into  the  tissue.  In  those  cases 
in  which  there  were  granulations  on  the  surface  they  were  com- 
posed of  neuroglia  alone. 

Marked  changes  in  the  neuroglia  of  the  cord  were  found  in 
but  one  case.  In  this  the  central  canal  was  dilated  and  around 
it  were  cell  aggregations.  The  blood  vessels  were  dilated,  and 
their  sheath  and  the  tissue  around  them  infiltrated  with  pus  cells. 
This  was  most  marked  in  the  gray  matter.  The  neuroglia 
cells  were  greatly  increased  in  number  in  the  gray  matter  of 
the  cord,  and  to  a  less  extent  in  the  white,  and  there  were 
numerous  nuclear  figures  within  them.      In  some  of  the  chronic 


109 


cases  there  was  thickening  of  the  neuroglia  around  the  periphery 
of  the  cord. 

These  neuroglia  changes  were  accompanied  by  changes  in  the 
connective  tissue.  The  cells  of  the  blood  vessels  were  swollen, 
increased  in  number  and  nuclear  figures  found  in  them.  In  the 
same  field  nuclear  figures  were  often  found  in  the  neuroglia  cells 
and  in  the  blood  vessels.  In  the  smaller  hsemorrhagic  foci 
the  walls  of  the  vessels  were  often  found  infiltrated  with  large 
epithelioid  cells,  together  with  lymphoid  and  plasma  cells.  This 
cellular  infiltration  was  most  marked  around  the  blood  vessels 
beneath  the  surface  of  the  ependyma.  A  definite  formation  of 
connective  tissue  proceeding  from  this  vascular  proliferation  was 
not  found  save  in  the  chronic  case  referred  to,  and  in  this  the 
process  had  advanced  so  far  that  the  steps  in  the  formation  of 
the  connective  tissue  could  not  be  followed.  In  this  same  case 
sections  through  the  indurated  areas  in  the  optic  thalamus 
showed  masses  of  fibrin  in  the  tissue  with  dense  cellular  aggre- 
gations. These  cell  masses  were  almost  entirely  composed  of 
plasma  cells,  with  a  few  lymphoid  cells  between  them. 

The  examination  of  the  ganglion  cells  for  degenerative  lesions 
was  the  least  satisfactory  part  of  the  work.  The  tissue  was 
examined  in  all  the  usual  methods  after  hardening  in  alcohol  and 
formaline.  In  many  of  the  cases  the  tissues  undoubtedly  re- 
mained too  long  in  the  hardening  fluid  before  examination. 
Changes  were  undoubtedly  present,  especially  in  the  most 
chronic  cases.  The  changes  found  consisted  in  an  alteration 
in  the  cell  granules,  combined  with  irregularity  in  shape  and 
often  atrophy  of  the  body  of  the  cell.  The  granules  in  some 
cases  were  absent,  in  others  in  place  of  the  large  angular 
granules  there  was  an  indistinct  fine  granulation.  In  some  of 
the  sections  which  were  hardened  in  Flemming's  solution  and 
in  some  hardened  in  Miiller's  fluid  and  subsequently  treated  by 
Marchi's  method  for  degeneration,  fatty  degeneration  was  found 
in  the  cell  protoplasm.  These  fat  granules  resulting  from  degen- 
eration could  be  distinguished  from  the  pigment  granules  of  the 
cells,  which  also  stain  with  osmic  acid,  by  their  greater  intensity  in 
staining,  their  irregular  size  and  irregular  distribution  in  the  cells. 


110 

In  addition  to  the  nerves,  portions  of  both  brain  and  cord  were 
treated  by  Marchi's  method  for  degeneration  in  the  nerve  fibres. 
Degeneration  to  some  degree  was  present  in  all  the  cases  ex- 
amined. In  sections  of  the  cortex  embracing  the  white  matter 
it  was  present  to  some  degree  but  was  not  marked.  Here  and 
there  in  the  white  matter  small  areas  of  degeneration  could  be 
seen.  In  those  sections  of  the  brain  which  embrace  the  internal 
capsule  the  degeneration  was  more  conspicuous.  The  degenera- 
tion was  much  more  marked  in  the  cord.  In  this,  it  was  most 
conspicuous  in  the  posterior  column  of  the  cord.  Under  a  low 
power  these  columns  were  often  almost  black  from  the  extent  of 
the  degeneration.  A  certain  amount  was  evident  in  the  pyramidal 
tracts  of  the  cord  and  in  the  antero-lateral  tract.  The  stain  for 
degeneration  was  of  importance  in  another  way,  —  in  bringing  out 
a  degeneration  of  the  swollen  cells  of  the  vessels,  which  was  often 
of  high  degree. 

Diplococci  were  found  in  variable  numbers  in  the  meninges  and 
in  the  brain  (Plate  III.,  Fig.  1).  They  were  always  most  numer- 
ous in  the  acute  cases,  where  the  exudation  was  composed  almost 
wholly  of  pus  cells.  Variable  numbers  were  found  in  the  single 
cells,  but  the  cells  wholly  filled  with  them  which  were  so  common 
in  the  alveoli  of  the  lungs  were  rarely  found.  In  the  chronic 
cases  prolonged  search  was  often  necessary  to  find  them  ;  in  the 
acute  cases  numbers  of  cells  containing  them  were  often  found 
in  a  single  field.  In  the  meninges  of  the  cord  they  seemed  to 
be  less  numerous  than  in  the  brain.  In  the  brain  they  seemed 
more  numerous  close  to  the  inner  surface.  They  were  also  found 
in  the  tissue  of  the  brain  in  those  acute  cases  in  which  there 
was  considerable  purulent  infiltration  of  the  tissue.  Here  they 
were  found  not  only  in  the  pus  cells  around  the  vessels,  but  in 
the  single  cells  in  the  interior  of  the  tissue. 

Lesions  in  the  Nerves  and  Ganglia. 

The   importance  of   the    study  of    the  nerve    lesions  was  only 

appreciated    in   the    latter   part  of   the  epidemic,  so  that  in  the 

earlier  cases  the  nerves  were  not   examined.     In    six   cases    the 

cranial  nerves,  including  the  Gasserian  ganglia,  were  examined, 


Ill 

and  in  two  cases  the  spinal  ganglia.  In  one  case,  in  addition 
to  the  cranial  nerves  a  number  of  peripheral  nerves  were 
examined  for  degeneration.  The  nerve  roots  of  the  spinal 
nerves  were  examined  in  the  sections  of  the  cord  in  every  case. 
Lesions  of  greater  or  less  degree  were  found  in  every  case 
examined,  and  seem  sufficiently  constant  to  justify  the  conclusion 
that  they  are  present  certainly  in  all  the  severe  cases. 

The  most  marked  lesions  were  found  in  the  second,  the  fifth 
and  eighth  nerves.  The  lesions  in  the  optic  nerves  represent  an 
extension  of  the  inflammatory  process  from  the  meninges.  The 
nerve  was  examined  in  cross  and  longitudinal  sections  from  the 
brain  to  its  entrance  into  the  eye.  The  dural  covering  of  the 
nerve  in  the  orbit  showed  little  change  save  dilatation  of  vessels. 
The  sub-dural  space  was  dilated,  but  usually  contained  no  cellular 
exudation.  Just  as  in  the  brain,  the  purulent  exudation  was 
found  in  the  pia-arachnoid  of  the  nerve.  The  connective  tissue 
of  this  was  infiltrated  with  pus,  and  there  were  masses  of  pus  cells 
in  the  membrane  and  in  spaces  chiefly  around  the  retinal  artery  after 
this  had  entered  into  the  sheath  (Plate  IV.,  Fig.  1).  The  blood 
vessels  of  the  nerve  itself  were  dilated,  the  space  between  the 
bundles  of  fibres  increased,  and  around  the  periphery  were  lines 
of  cellular  infiltration  which  extended  from  the  outside  between 
the  bundles  of  fibres.  In  a  longitudinal  section  of  the  nerve, 
involving  a  part  of  the  retina,  the  infiltration  could  be  followed 
from  the  meninges  of  the  nerve  into  the  eye.  Another  longitu- 
dinal section  of  the  nerve  in  one  case  showed  a  small  mass  of  pus 
cells  lying  in  the  sub-dural  space  and  the  dura  immediately  over 
this  was  infiltrated  with  cells.  In  the  acute  cases  the  cells  in  the 
meninges  of  the  nerve  extending  between  the  nerve  bundles  were 
polynuclear  leucocytes.  The  degree  of  the  infiltration  varied. 
In  one  case  considerable  numbers  of  leucocytes  were  found 
extending  almost  to  the  centre  of  the  nerve.  In  more  chronic 
cases  along  with  the  pus  cells  there  were  numerous  large  epithelioid 
cells  similar  to  those  found  in  the  meninges  of  the  brain.  Around 
the  vessels  there  were  very  few  lymphoid  and  plasma  cells. 
Changes  similar  to  those  in  the  optic  nerve  were  found  in  the 
olfactory  nerve  and  the  bulb,  but  the  cellular  infiltration  between 


112 

the  nerve  bundles  was  not  so  marked.  It  was  very  interesting  to 
find  in  both  the  optic  and  olfactory  nerve  proliferative  changes  in 
the  neuroglia  cells  similar  to  those  described  in  the  brain.  In  one 
case  of  five  days'  duration  nuclear  figures  in  great  variety  and 
beauty,  showing  centresomes  and  spindles,  were  found  in  the 
neuroglia  cells  (Plate  VII.,  Figs.  2  and  3).  Two  such  figures 
were  sometimes  seen  in  the  same  field.  Cells  with  granular  proto- 
plasm and  two  or  more  nuclei  were  also  seen. 

Sections  of  the  eighth  nerve  (Plate  V.,  Fig.  1)  in  acute  cases 
showed  the  nerve  embedded  in  a  mass  of  pus,  the  nerve  sheath 
softened,  broken  up  and  in  places  entirely  lost.  The  nerve  itself 
was  infiltrated  with  enormous  numbers  of  pus  cells,  partly  in  the 
form  of  lines  running  through  it,  partly  as  a  more  diffuse 
infiltration.  In  some  sections  the  nerve  was  broken  up,  greatly 
swollen  and  the  single  bundles  of  fibres  separated  by  large 
accumulations  of  cells.  Here  also  in  acute  cases  only  pus  cells 
were  found  around  the  invading  nerve,  and  in  the  more  chronic 
cases  there  were  fewer  pus  cells,  and  in  the  place  of  them  lines  of 
epithelioid  and  plasma  cells.  The  seventh  nerve  frequently  showed 
as  great  degree  of  infiltration  as  the  eighth.  Some  infiltration 
was  also  found  along  the  third  and  sixth  nerves,  but  it  was  not  so 
marked.  In  one  case  longitudinal  sections  of  the  fourth  nerve 
were  made,  and  showed  no  infiltration. 

Longitudinal  sections  of  the  fifth  nerve,  involving  the  ganglion 
and  some  of  the  peripheral  branches,  showed  an  intense  neuritis 
on  the  cerebral  side  of  the  ganglia.  The  single  bundles  of  fibres 
were  widely  separated  from  one  another,  and  between  them  there 
was  considerable  exudation,  in  which  there  were  numbers  of  pus 
cells  and  epithelioid  cells.  The  cellular  infiltration  did  not  seem 
to  extend  so  diffusely  into  the  nerve  bundles  as  it  did  in  the  case 
of  the  eighth  nerve.  These  exudative  changes  were  accompanied 
in  the  fifth  nerve,  as  in  the  spinal  nerve,  by  a  considerable  degree 
of   cellular  proliferation. 

Sections  of  the  nerve  roots  (Plate  IV.,  Fig.  2)  of  the  spinal  cord 
showed  that  these  were  affected  in  every  case,  but  there  was  a  great 
deal  of  difference  in  the  extent  of  the  lesions.  As  a  rule,  the 
greatest  degree  of  affection  of  the  nerve  roots  was  found  in  that 


113 

part  of  the  cord  where  the  cellular  infiltration  was  greatest, 
although  in  some  cases  a  considerable  degree  of  involvement  of 
the  nerve  roots  was  found,  with  very  little  infiltration  of  the 
meninges.  In  most  of  the  acute  cases  the  lesions  in  the  nerve 
roots,  as  shown  on  cross  and  oblique  sections,  were  of  the  same 
character  as  those  seen  in  the  cranial  nerves.  There  was  a  marked 
degree  of  dilatation  of  the  blood  vessels,  the  peri-neurium  was 
infiltrated  with  pus  cells,  the  nerve  was  swollen,  the  separate 
bundles  of  fibres  separated  from  one  another  by  spaces  in  which 
there  was  considerable  cellular  infiltration.  Even  in  the  most 
acute  cases  these  changes  were  accompanied  b}^  proliferative 
changes  in  the  peri-  and  endo-  neurium.  The  cells  of  the  blood 
vessels  were  swollen,  increased  in  number,  and  around  the  blood 
vessels  along  with  the  pus  cells  there  were  numbers  of  large 
epithelioid  and  plasma  cells.  The  lymphoid  cells  were  compara- 
tively few  in  number.  Nuclear  figures  were  often  found  in  the 
epithelioid  and  plasma  cells.  Not  only  were  these  changes  found 
in  the  peri-neurium  and  in  the  small  bundles  of  connective  tissue 
separating  the  larger  bands  of  nerve  fibres,  but  small  collections 
of  plasma  and  lymphoid  cells  were  occasionally  found  within  the 
nerve  bundles  and  between  the  fibres  (Plate  VII.,  Fig.  1).  All 
of  these  changes  were  more  marked  in  the  posterior  than  in  the 
anterior  roots. 

In  some  of  the  more  chronic  cases  lesions  in  the  spinal  nerve 
roots  were  more  marked  than  in  the  acute.  Around  all  of  the 
blood  vessels,  even  the  smallest,  there  was  an  intense  prolifera- 
tion of  cells,  which  so  extended  between  the  single  nerve  fibres 
that  in  places  these  seemed  to  be  entirely  destroyed.  The  cells 
belonged  principally  to  the  type  of  plasma  cells.  The  greatest 
amount  of  nerve  degeneration,  as  shown  by  the  Marchi  method, 
was  found  in  the  optic  nerve  in  one  case  (Plate  VII.,  Fig.  2), 
and  in  the  eighth  nerve  in  another.  Sections  of  the  optic  nerve 
under  the  low  power  were  very  dark  from  the  masses  of  fatty 
degenerated  myelin  stained  black  with  osmic  acid.  With  a  high 
power  in  some  of  the  bundles  a  large  number  of  the  single  nerve 
fibres  were  found  to  be  affected.  The  degeneration  was  almost 
as  marked  in  the  seventh  nerve.     In   a  longitudinal  section  of 


IM 

the  nerve,  in  which  the  degeneration  of  the  single  fibres  could 
easily  be  followed,  a  count  showed  in  one  place  three-fourths  of 
the  fibres  to  be  affected.  In  most  of  the  nerves  in  which  the 
myelin  was  swollen  and  broken  up  the  axis  cylinder  was  swollen, 
transparent  or  entirely  absent. 

Longitudinal  section  of  the  optic  nerve  from  the  same  case  did 
not  show  so  great  degree  of  involvement.  In  every  case  degen- 
eration was  found  in  the  spinal  nerve  roots,  and  was  more  marked 
in  the  posterior  than  in  the  anterior  roots  (Plate  VIII.,  Fig.  1). 
Only  in  one  case  was  there  an  extensive  examination  of  the 
peripheral  nerves  for  degeneration.  A  minor  degree  of  degen- 
eration was  found  in  the  nerves  of  the  cauda  equina  and  in 
the  popliteal  nerves.  A  considerable  degree  was  found  in  the 
same  case  in  the  seventh  nerve.  The  fifth  nei've  was  only 
examined  in  one  case,  in  which  there  had  been  great  involve- 
ment of  the  ganglia,  and  in  this  extensive  degeneration  was  found. 

In  one  of  the  cases  a  section  treated  for  degeneration  was 
taken  through  all  the  nerves  and  muscles  of  the  orbit.  All 
of  the  nerves  showed  more  or  less  marked  degenerative  changes, 
but  the  optic  nerve,  and  next  to  this  the  branches  of  the  sixth, 
seemed  to  be  most  affected.  The  muscles  of  the  section  showed 
advanced  fatty  degeneration.  Sections  of  the  spinal  cord  stained 
by  Weigert's  method  show  equally  the  destruction  of  the  nerve 
roots.  In  one  chronic  case  comparatively  few  intact  nerve 
fibres  were  found. 

In  five  cases  sections  were  made  of  the  Gasserian  ganglia, 
and  in  two  of  the  spinal  ganglia.  The  Gasserian  ganglia 
in  the  acute  cases  were  infiltrated  with  pus,  and  masses  of  gan- 
glion cells  were  often  separated  from  their  connection  (Plate  V., 
Fig.  2).  Even  single  ganglion  cells  were  often  found  lying 
free  in  the  exudation.  Along  with  the  purulent  exudation 
there  was  more  or  less  haemorrhage .  Many  of  the  ganglion 
cells,  especially  those  most  distant  from  the  exudation,  seemed  to 
be  normal.  Others  were  small,  their  outline  exceedingly  irreg- 
ular, the  nucleus  pale  or  in  some  cases  absent  altogether.  Small 
irregular  masses,  representing  completely  necrotic  ganglion  cells, 
were  often  found.      In  the  most  marked  cases  the  granulation 


115 

of  all  of  the  cells  was  iudistinct.  The  cells  also  often  con- 
tained large  vacuolar  spaces.  The  diplococci  were  found  in  the 
pus  cells  infiltrating  the  optic  nerve  and  in  the  infiltration  of 
the  pia-arachnoid  around  it.  In  several  cases  they  were  found 
in  the  sections  of  the  Gasserian  ganglia,  but  were  not  found  in 
the  sections  of  the  spinal  ganglia.  In  one  case  they  were  found 
in  the  olfactory  nerve  and  in  the  auditory  in  one.  They  were 
not  found  in  the  other  nerves  or  in  the  nerve  roots  of  the 
spinal  cord.  No  leucocj-tes  were  found  in  the  necrotic  ganglion 
cells.  In  the  more  chronic  cases  the  amount  of  leucocytic  in- 
filtration was  less,  and  throughout  the  ganglia  there  were  large 
numbers  of  cells  which  came  from  proliferation  of  the  connective 
tissue.  In  one  case  the  ganglion  appeared  to  be  oedematous. 
The  tissue  was  loose  and  the  single  cells  widely  separated  from 
one  another  both  by  cellular  infiltration  and  by  the  oedema. 
Immense  numbers  of  newly  formed  cells  were  found  around 
the  ganglion  cells.  The  cellular  investment  of  the  single  cells 
was  in  most  cases  much  thicker,  and  the  cells  were  swollen  and 
many  took  on  an  epithelioid  character.  Nuclear  figures  were 
found  in  the  surrounding  cells.  The  cells  lying  in  the  tissue 
between  these  ganglion  cells  often  had  the  character  of  plasma 
cells.  There  were  also  considerable  numbers  of  lymphoid  cells. 
The  same  condition  of  atrophy  of  the  cells,  often  going  into 
complete  necrosis,  was  found  here  as  in  the  acute  cases.  The 
spinal  ganglia  were  not  equally  affected.  This  was  apparent 
on  macroscopic  examination.  All  seemed  to  be  somewhat 
swollen  and  oedematous,  but  in  some  this  condition  was  much 
more  marked  than  in  others.  On  microscopic  examination  much 
the  same  changes  were  found  in  these  as  in  the  Gasserian 
ganglia.  The  blood  vessels  were  injected  and  the  ganglion 
infiltrated  with  pus.  There  was  proliferation  of  the  cells  about 
the  blood  vessels  and  of  the  cells  about  the  ganglion  cells. 
The  ganglion  cells  were  often  separated  from  their  connection 
and  lying  in  the  exudation.  These  were  irregular  in  shape 
and  the  nucleus  stained  imperfectly  or  not  at  all.  Others  showed 
the  same  degenerative  lesions  as  have  been  described  in  the 
Gasserian  ganglion   (Plate  VI.,  Fig.   1).      Sections  of  the  gan- 


116 

glion,  including  longitudinal  section  of  the  nerve  roots  in  con- 
nection with  it,  showed  these  infiltrated  with  pus.  The  rapidity 
with  which  these  changes  can  take  place  was  shown  in  a  sec- 
tion of  the  ganglia  in  the  goat  which  died  not  later  than  twelve 
hours  after  inoculation  in  the  spinal  canal  with  a  pure  culture 
of  the  diplococcus.  In  one  of  the  ganglia  there  was  beginning 
purulent  infiltration.  There  seems  little  doubt  that  in  both 
the  spinal  and  Gasserian  ganglia  the  condition  is  due  to  direct 
extension  along  the  nerves.  There  were  no  lesions  in  a  small 
sympathetic  ganglion  found  in  one  of  the  sections  through  the 
orbit.  In  one  case,  in  which  sections  of  the  Gasserian  gan- 
glion and  the  nerves  showed  a  very  extensive  neuritis,  sections 
were  made  through  the  olfactory  bulb.  This  was  swollen  and 
in  places  intensely  infiltrated  with  cells  among  which  were  many 
pus  cells,  but  the  cells  seemed  to  come  principally  from  pro- 
liferation. The  tissue  was  (Edematous  and  the  large  triangular 
nerve  cells  often  appeared  atrophied.  Sections  passing  through 
the  olfactory  nerve  from  the  same  case  showed  a  considerable 
degree  of  degeneration. 

Sections  of  the  eye  were  examined  in  two  cases,  in  one  of  which 
choroiditis,  cloudiness  of  cornea  and  conjunctivitis  were  ascer- 
tained during  life.  The  sections  embraced  in  this  case  the  fundus 
of  the  eye  through  the  entrance  of  the  optic  nerve,  the 
ciliary  region  and  the  cornea.  The  sections  through  the  optic 
nerve  and  fundus  showed  a  marked  infiltration  of  the  nerve 
sheath  up  to  its  entrance  into  the  eye.  Where  the  nerve  sheath 
was  lost  in  the  eye  there  was  a  considerable  accumulation  of 
pus  cells,  with  proliferation  of  the  adjoining  tissue  cells.  From 
this  point  an  infiltration  with  leucocytes  extended  directly  into 
the  eye.  The  optic  nerve  was  swollen,  the  spaces  between  the 
fibres  increased,  and  in  these  spaces  an  occasional  pus  cell 
and  cells  of  new  formation  were  found.  All  of  the  vessels  of 
the  choroid  were  intensely  injected,  but  there  were  few  haemor- 
rhages and  no  infiltration  with  pus  cells  in  this.  The  retina 
on  either  side  of  the  entrance  of  the  optic  nerve  was  broken 
up  and  infiltrated  with  pus.  Further  up  the  retina  was  in  places 
very  well  preserved,  but  generally  nothing  could  be  seen  of  the 


117 

layer  of  rods  and  cones.  The  tissue  was  infiltrated  with  pus 
cells  and  haemorrhage,  and  in  places  the  entire  retina,  with  the 
exception  of  the  granular  layer  immediately  beneath  the  rods 
and  cones,  was  destroyed.  All  the  blood  vessels  of  the  retina 
were  intensely  injected,  and  in  places  there  was  a  considerable 
amount  of  fibrin  around  them.  Notwithstanding  the  enormous 
congestion  of  the  blood  vessels  of  the  choroid,  no  diapedesis 
seemed  to  take  place  from  them  and  in  none  of  them  was  there 
an  accumulation  of  leucocytes.  Only  in  a  few  places  scattered 
leucocytes  were  found  in  the  tissue  of  the  choroid.  The  tissue 
appeared  to  be  looser  than  normal,  and  in  the  loose  meshes  of 
the  tissue  epithelioid  cells  with  nuclear  figures  were  found.  The 
vitreus  was  filled  with  a  large  amount  of  pus  made  up  entirely 
of  polynuclear  leucocytes,  none  of  them  containing  eosinophile 
granules.  The  largest  mass  of  this  pus  was  adherent  to  the 
retina  and  to  the  iris.  The  anterior  chamber  contained  a  large 
amount  of  pus.  The  tissue  of  the  iris  was  oedematous  and 
infiltrated  with  pus  cells.  The  blood  vessels  were  injected. 
The  pigment  cells  were  broken  up,  the  pigment  scattered  in  the 
tissue,  and  the  pus  cells  in  the  iris  and  in  the  anterior  chamber 
were  loaded  with  pigment  derived  from  this  destruction  of  cells. 
A  considerable  amount  of  reticular  fibrin  and  numbers  of  red 
blood  corpuscles  were  found  among  the  pus  cells  in  the  anterior 
chamber.  No  evidences  of  proliferation  were  seen  in  any  of 
the  pigment  cells  of  the  iris  or  ciliary  region.  In  the  ciliary 
region  the  blood  vessels  were  injected,  the  tissue  was  swollen, 
oedematous  and  infiltrated  both  with  pus  cells  and  with  cells  arising 
from  proliferation.  The  sclera  was  normal,  except  at  the  corneal 
attachment.  There  all  of  the  blood  vessels  were  injected,  and 
it  contained  large  numbers  of  pus  cells  and  epithelioid  cells. 
The  cells  of  the  vessels  were  swollen,  and  nuclear  figures  were 
found  in  them.  The  section  passing  through  the  cornea  showed 
the  fibres  of  this  separated,  and  the  tissue  contained  a  great 
many  pus  cells  lying  in  the  corneal  spaces.  At  its  commence- 
ment the  cornea  was  almost  homogeneously  infiltrated,  further 
along  toward  the  middle  a  few  pus  cells  were  found  in  the 
posterior  portion  of  the  cornea  and  they  seemed  most  abundant 


118 

in  the  middle.  The  epithelium  was  almost  entirely  lost  over 
the  posterior  surface  of  the  cornea,  and  over  the  anterior  sur- 
face it  was  for  the  most  part  reduced  to  single  cells.  In  this 
case  the  duration  of  the  disease  was  seven  days.  In  the  other 
eye  examined,  coming  from  a  case  of  three  days'  duration,  the 
lesions  were  not  so  marked.  The  vessels  of  the  choroid  were 
intensely  injected,  and  here  and  there  a  slight  amount  of 
haemorrhage  and  cellular  infiltration  was  found.  The  retina 
was  separated,  the  vessels  were  intensely  injected,  and  a  few 
slight  haemorrhages  were  found.  The  different  layers  of  the 
retina  were  usually  made  out,  and  appeared  to  be  but  little 
changed. 

In  the  eye  first  described  a  portion  of  the  conjunctiva  was  cut 
at  the  same  time  with  the  eye.  All  of  the  blood  vessels  in  this 
were  intensely  injected  and  there  was  a  great  deal  of  hsemorrhage 
in  the  tissue  which  seemingly  came  from  the  small  vessels.  The 
tissue  was  infiltrated  with  pus  cells  which  extended  up  into  the 
epithelium.  The  spaces  in  the  tissue  beneath  were  increased,  and 
it  was  evidently  oedematous.  About  the  vessels  in  the  spaces  in 
the  tissue  there  were  large  numbers  of  plasma  cells  and  occasional 
groups  of  epithelioid  cells.  Nuclear  figures  were  found  in  both 
in  small  numbers.  Diplococci  were  found  in  considerable  numbers 
in  the  pus  cells  in  the  vitreous  and  in  the  anterior  chamber.  In 
one  section  a  few  were  found  in  the  retina.  None  were  found  in 
the  cornea  or  in  the  iris.  In  the  acute  case  it  was  easy  to  trace 
the  organisms  from  the  brain  along  the  optic  sheaths  to  the  eye. 

Pituitary  Body. 
In  two  cases  the  pituitary  body  was  examined.  Sections  pass- 
ing through  the  pedicle  showed  a  purulent  infiltration  extending 
around  this  and  down  into  the  gland.  At  the  periphery  of  the 
gland  in  one  place  the  exudation  extended  down  into  the  tissue 
and  there  was  necrosis  and  atrophy  of  the  glandular  elements. 

Nose. 
In  three  cases  sections  of  the  mucous  membrane  of  the  upper 
air  passages  were  examined.     Two  were  normal  and  in  one  there 


119 

was  a  purulent  infiltration  of  the  mucous  membrane  and  of  the 
sub-mucous  tissue  with  intense  hypersemia  of  the  blood  vessels. 
A  few  single  pairs  of  diplococci  were  found  in  the  pus  cells.  In 
this  case  microscopic  examinations  of  the  nasal  secretion  from  the 
nose  during  life  were  positive,  showing  diplococci  in  the  pus  cells. 

Lungs. 

The  condition  of  the  lungs  is  interesting,  on  account  of  the 
relation  which  has  very  generally  been  supposed  to  exist  between 
acute  epidemic  cerebro-spinal  meningitis  and  pneumonia.  In 
thirteen  cases  there  was  merely  congestion,  with  more  or  less 
oedema.  In  a  few  of  the  cases  the  oedema  was  well  marked.  In 
seven  cases  there  was  broncho-pneumonia,  most  marked  in  the 
lower  posterior  portions  of  the  lung,  with  more  or  less  bronchitis. 
In  two  cases  there  was  characteristic  croupous  pneumonia,  one  in 
the  stage  of  red  hepitazation  bordering  on  gray.  There  was  a 
fibrinous  pleurisy  over  the  consolidated  lung.  Pneumococci  were 
found  in  cultures  and  on  microscopic  examination.  In  eight  cases 
a  pneumonia  due  to  the  diplococcus  was  found.  Nearly  all  of 
these  cases  come  from  the  last  part  of  the  epidemic.  It  is  very 
possible  that  in  some  of  the  earlier  cases  in  which  the  lesions  were 
described  simply  as  broncho-pneumonia,  they  were  really  due  to  the 
diplococcus.  The  lung  lesions  in  cases  which  are  described  as 
broncho-pneumonia  with  bronchi-ectatic  cavities,  and  foci  of  con- 
solidation with  necrosis  and  breaking  down,  may  also  have  been 
due  to  the  diplococcus.  The  lesions  macroscopically  consisted 
of  areas  of  consolidation  in  various  parts  of  the  lung,  more  par- 
ticularly in  the  lower  lobe  and  they  were  most  numerous  beneath 
the  pleural  surface.  The  foci  varied  in  size  from  a  pin's  head 
up  to  that  of  a  bean,  and  on  section  some  of  them  resembled 
small  hsemorrhages  in  the  tissue.  In  other  cases  the  periphery 
of  the  area  was  distinctly  haemorrhagic  and  the  centre  opaque 
and  yellowish.  The  number  of  these  areas  varied.  In  some 
of  the  cases  but  few  were  found,  in  others  they  were  numerous. 
In  one  case  the  consolidation  in  the  lung  was  so  extensive  that 
it  might  easily  have  been  regarded  as  croupous  pneumonia,  par- 
ticularly as  the  pleura  over  it  was  covered  with  a  definite  fibrinous 


120 

exudation.  On  section  the  large  area  was  composed  of  a  number 
of  irregular  grayish  foci  with  softened  centres  and  with  haemor- 
rhagic  and  oedematous  tissue  between  them. 

The  lung  tissue  in  the  yellowish  centres  was  frequently  broken 
down,  and  pus  oozed  from  this.  The  bronchi  in  these  places 
contained  more  or  less  muco-purulent  material,  but  there  did  not 
seem  to  be  that  relation  between  the  bronchi  and  the  areas  of 
consolidation  which  is  found  in  broncho-pneumonia. 

On  microscopic  examination  the  central  areas  showed  in  most 
cases  a  purulent  infiltration  of  the  tissue,  breaking  down  and 
beginning  abscess  formation.  In  the  centres  there  were  large 
numbers  of  pus  cells  in  the  alveoli.  The  walls  of  the  alveoli  were 
thin,  infiltrated  with  pus  and  in  places  entirely  broken  down. 
Surrounding  this  the  purulent  infiltration  was  not  so  intense  and 
around  the  outside  there  was  often  oedema  with  a  slight  amount  of 
hsemorrhage.  Some  of  the  foci  were  distinctly  hasmorrhagic,  with 
areas  here  and  there  of  purulent  infiltration.  The  exudation  in 
the  alveoli  in  the  centres  contained  nothing  but  pus  cells. 
Further  out  mixed  with  the  pus  cells  there  were  numbers  of  large 
cells  similar  to  those  in  the  brain,  and  they  often  enclosed  the  pua 
cells.  These  large  cells  were  also  found  in  the  more  oedematous 
portions.  In  addition  to  the  exudation,  at  the  periphery  there 
was  some  cellular  proliferation  of  the  tissue  of  the  lung.  There 
were  plasma  and  epithelioid  cells  about  the  blood  vessels,  and  the 
cells  lining  the  walls  of  the  alveoli  were  swollen.  In  one  case 
nuclear  figures  in  small  numbers  were  found  in  these  cells.  The 
exudation  in  the  lung,  as  in  the  brain,  was  characterized  by  the 
absence  of  eosinophile  cells.  On  microscopic  examination  the 
foci  of  consolidation  did  not  appear  to  be  bronchial  in  origin. 
The  bronchi  in  the  vicinity  often  contained  pus  cells,  but  their 
walls  were  not  infiltrated.  The  duration  of  the  disease  in  the 
cases  in  which  diplococcus  pneumonia  was  found  was  :  in  twa 
cases,  three  days ;  in  one  case,  two  days  ;  in  one,  five  days;  in 
one,  nine  days ;  in  one,  twenty-three,  one  seventy-four  and  one 
five  days.  The  average  duration  was  fifteen  and  one-half  days. 
It  will  be  seen  from  these  figures  that  the  lung  complications  due 
to  the  diplococcus  can  take  place  in  almost  any  period  of  the 


121 

disease.  In  the  case  of  seventy-four  days'  duration  the  lesions  in 
the  brain  and  cord  could  be  regarded  as  almost  completely  healed, 
and  the  lesions  in  the  lung  were  acute.  In  one  case,  in  which  the 
apparent  history  of  the  disease  was  only  of  two  days'  duration, 
the  lung  lesions  were  so  advanced  that  they  seemed  possibly  to 
antedate  those  of  the  brain,  providing  the  history  as  given  by  the 
patient's  relatives  was  accurate. 

Immense  numbers  of  diplococci  were  found  in  the  pus  cells  in 
these  places  (Plate  III.,  Fig.  2).  They  were  most  numerous  in 
the  cells  in  the  centres  of  the  foci,  where  the  softening  of  the 
tissues  was  taking  place.  Sometimes  in  an  alveolus  every  pus 
cell  was  almost  filled  with  them.  With  low  power  the  places 
containing  them  in  greatest  abundance  could  be  easily  recognized 
by  the  dark  color  which  their  presence  gave  to  the  cells.  They 
were  found  exclusively  in  the  cells.  Although  most  numerous  in 
these  places,  they  were  also  found  in  the  pus  cells  in  considerable 
numbers  around  the  periphery  of  the  central  area  and  in  the 
scattered  pus  cells  of  the  oedematous  portion.  None  were  found 
in  any  of  the  large  cells,  but  occasionally  a  few  swollen  and 
imperfectly  stained  forms  were  found  in  the  pus  cells  enclosed  in 
these.  In  the  centre  of  one  of  the  foci  a  small  branch  of  the 
pulmonary  artery  occluded  by  a  thrombus  formed  of  pus  cells 
enclosing  large  numbers  of  diplococci  was  found.  It  seemed 
probable  that  this  thrombus  may  have  come  as  an  embolus  from 
the  meninges  and  may  have  produced  the  infection  of  the 
surrounding  tissue.  The  organisms  were  also  found  in  the  pus 
cells  in  some  of  the  bronchi  within  the  consolidated  areas,  but 
they  were  not  found  in  the  bronchi  at  a  distance.  The  peri- 
vascular lymphatics  were  dilated  and  contained  coagulated 
material,    pus   and    fibrin. 

Spleen. 
There  is  a  great  variation  in  the  size  of  the  spleen.  In 
general  it  is  not  much  enlarged,  and  is  probably  smaller  than 
in  most  of  the  acute  infectious  diseases.  In  only  three  cases 
was  it  found  considerably  enlarged  ;  in  one  of  these  it  weighed 
four  hundred  and  ten  gms.,  in    one    three    hundred   and  seven 


122 

and  in  one  three  hundred  and  two  gms.  The  average  weight 
of  the  adnlt  cases  was  one  hundred  and  sixty-three  gms.  It 
is  rather  remarkable  that  in  the  two  acute  cases  complicated 
with  croupous  pneumonia  the  spleen  should  have  weighed  in 
one  eighty  gms.  and  in  the  other  eighty-five  gms.  The  small 
spleen  was  normal  on  histological  examination.  In  the  largest 
spleen,  which  was  macroscopically  rather  soft,  there  was  no  en- 
largement, but  rather  a  diminution  in  the  size  of  the  malpighian 
bodies,  with  considerable  diminution  in  the  lymphoid  cells.  In- 
creased size  of  the  spleen  was  due  chiefly  to  acute  hypersemia. 
At  the  beginning  of  our  study  of  the  disease  we  were  of  the 
opinion  that  the  smallness  of  the  spleen  could  serve  clinically 
as  a  differential  mark  in  distinguishing  this  form  of  meningitis 
from  the  pneumococcus  form,  but  a  small  size  is  not  suflSciently 
constant  to  be  of  service  clinically.  In  some  of  the  more  chronic 
cases  the  capsule  of  the  spleen  was  wrinkled,  showing  that  the 
spleen  had  been  larger.  The  average  duration  of  disease  in 
the  three  cases   of  enlarged  spleen  was  five  days. 

Lymphatic  Glands. 
The  lymphatic  glands  in  the  uncomplicated  cases  were  never 
found  enlarged.     Microscopically  the  blood  vessels  were  injected, 
but  there  was  no  alteration  in  the   histological  structure  of  the 
gland  and  no  dilatation  of  the  lymph  spaces. 

Liver. 
The  liver  presented  but  little  abnormal.  It  was  generally 
rather  pale  and  cloudy  on  section.  In  three  cases  microscop- 
ically there  was  slight  increase  in  the  fibrous  tissue,  with  cellular 
infiltration.  In  one  case,  where  it  was  enlarged,  the  cells  were 
swollen,  granular  and  fatty,  and  there  were  numbers  of  leucocytes 
in  the  capillaries.  In  one  case  there  were  foci  of  purulent  infiltra- 
tion in  the  enlarged  portal  spaces.  There  were  no  foci  of  necrosis 
such  as  are  sometimes  found  in  some  of  the  infectious  diseases. 

Kidneys. 
In  two  cases  acute  lesions  were  found  in  the  kidney.     In  one  of 
these  the  kidney  lesion  had  nothing  to  do  with  the  meningitis,  the 


128 

boy  having  become  infected  with  diphtheria,  of  which  he  died, 
after  having  practically  recovered  from  the  meningitis.  The 
kidneys  in  this  case  were  swollen,  the  glomeruli  enlarged  and 
opaque,  showing  as  yellowish  points.  Under  a  low  power  the 
glomeruli  were  prominent.  About  most  of  them  there  was  a  darkly 
stained  mass,  composed  of  fibrin  and  blood.  The  interstitial 
tissue  was  dilated.  With  high  power  the  convoluted  tubules  were 
everywhere  swollen,  in  some  places  entirely  filling  up  the  lumen, 
and  the  cells  in  some  places  were  filled  with  hyaline  granules. 
In  a  large  number  of  tubules  there  was  haemorrhage,  and  in  places 
they  were  filled  with  masses  of  definite  fibrin.  In  a  few  places 
in  the  intermediate  zone  of  the  kidney  there  were  found  both 
in  the  vessels  and  in  the  interstitial  tissue  the  large  cells 
characteristic  of  acute  interstitial  nephritis.  Around  most  of 
the  glomeruli  there  was  a  mass  of  fibrin,  partly  reticular,  partly 
converted  into  hyaline  masses.  In  places  in  the  glomeruli  groups 
of  vessels  were  necrotic  and  here  and  there  were  haemorrhage 
and  leucocytes  with  broken-down  nuclei  in  the  tissue.  Some 
of  the  glomeruli  were  completely  necrotic.  The  haemorrhage  and 
fibrinous  material  in  the  capsules  of  the  glomeruli  extended  into 
the  tubules  leading  off  from  them.  The  kidney  lesions  in  this 
case  should  be  attributed  not  to  the  meningitis  but  to  the  diph- 
theria, although  such  glomeruli  lesions  are  extremely  uncommon  in 
diphtheria.  In  this  case  there  was  complete  anuria  for  two  days 
before  death. 

In  one  other  case  there  was  acute  haemorrhagic  nephritis. 
In  this  case  there  was  an  accompanying  acute  pericarditis,  the 
organisms  causing  which  could  not  be  ascertained.  In  two 
cases  there  was  a  minor  degree  of  chronic  interstitial  nephritis. 
The  only  lesions  found  in  the  kidneys  which  could  be  properly 
attributed  to  the  meningitis  were  acute  degenerative  lesions, 
which  were  always  present.  In  one  case  there  was  an  abcess 
in  the  seminal  vesicles.  The  case  was  accompanied  by  croupous 
pneumonia,  and  on  both  cover-slip  examination  of  the  contents, 
and  in  the  cultures  only  pneumococci  were  found.  On  micro- 
scopic examination,  in  addition  to  the  numerous  pneumococci  a 
small  number  of  swollen  and  degenerated  diplococci  were  found 
in  the  pus  cells. 


124 


Intestinal  Canal. 

The  intestinal  canal  was  found  normal  in  every  case  save  in 
the  case  accompanied  by  diphtheria,  and  in  this  the  usual 
swelling  of  the  follicles  was  found.  This  is  interesting  in  view 
of  the  fact  that  swelling  of  the  follicles  and  even  ulceration  have 
been  described  in  the  disease. 

In  one  case  an  abscess  of  the  tonsil  was  found,  in  which 
characteristic  diplococci  were  found  on  cover-slip  examination 
and  cultures.     No  sections  of   this  were  examined. 

Heart. 
The  heart  was  not  examined  microscopically  as  a  matter  of 
routine.  In  several  cases  in  which  sections  were  made  of  it 
it  was  found  normal.  In  two  cases  there  was  an  acute  peri- 
carditis, combined  in  one  case  with  foci  of  necrosis  and  purulent 
infiltration  in  the  myocardium.  No  diplococci  were  found  in 
connection  with  these  lesions. 

Skin  Lesions. 
Lesions  of  the  skin  were  found  in  but  one  of  the  cases  which 
came  to  autopsy.  In  this  case  over  upper  and  lower  extrem- 
ities, chest  and  abdomen  there  were  numerous  small,  dark 
purplish  spots  in  the  skin,  varying  in  size  from  a  pin's  head 
up  to  that  of  a  pea.  The  smaller  ones  were  not  elevated 
above  the  surface.  In  many  of  the  larger  ones  the  centres  were 
more  opaque  and  slightly  elevated.  They  could  not  be  made 
to  disappear  on  pressure,  but  remained  more  sharply  marked, 
the  blood  being  pressed  from  the  surrounding  hypersemic  vessels. 
On  microscopic  examination  of  these  areas  there  was  intense 
congestion  and  dilatation  of  the  blood  vessels  of  the  skin  in 
the  area  and  in  the  surrounding  skin.  Immediately  beneath 
the  epithelium  there  were  small  and  diffuse  haemorrhages.  In 
the  deeper  tissue  about  the  sweat  glands  and  extending  down 
into  the  fat  the  haemorrhages  were  more  diffuse  and  more 
extensive.  The  largest  hsemorrhages  were  found  in  the  sub- 
cutaneous fat.     The   deep   vessels   of   the   skin    and  the  vessels 


125 

of  the  fat  were  intensely  congested.  There  was  some  prolif- 
eration around  the  superficial  blood  vessels  throughout  the  entire 
area.  In  the  centre  corresponding  to  the  area  of  haemorrhagic 
infiltration  beneath  the  epithelium  there  was  some  infiltration 
with  pus  cells.  In  the  larger  areas  with  a  yellowish  centre  the 
epithelium  was  infiltrated  with  pus,  and  one  of  the  specimens 
showed  the  upper  layers  of  the  epithelium  slightly  elevated  by 
the  accumulation  of  pus  cells  beneath.  No  diplococci  were 
found  in  the  pus  cells  in  these  areas.  In  one  case  the  herpetic 
vesicles  on  the  lip  were  examined.  In  them  there  was  an  intense 
infiltration  with  pus  cells  in  the  tissue  around  the  vessels  with 
proliferation  of  the  fixed  cells  of  the  tissue.  Here  also  no 
diplococci  were  found  in  the  pus  cells. 


CLASSIFICATION   OF   THE   DISEASE. 

Hirsch^^  divides  the  disease  into  the  following  form :  — 

1.  Meningitis  cerebro-spinalis  epidemica  siderans. 

2.  Meningitis  cerebro-spinalis  epidemica  abortiva. 

3.  Meningitis  cerebro-spinalis  epidemica  intermittens. 

4.  Meningitis  cerebro-spinalis  epidemica  typhoides. 
Striimpel,^"  while   in   the  main  adopting   the   classification   of 

Hirsch,  thinks  that  the  so-called  abortive  form  should  include 
the  mild  cases  which  begin  with  the  phenomena  of  the  disease 
in  an  intense  form  and  which  rapidly  recover. 

While  recognizing  the  futility  of  attempts  to  classify  a  dis- 
ease, it  would  probably  be  well  for  practical  purposes  to  recog- 
nize certain  types,  the  differences  between  which  depend  on  the 
intensity  and  duration  of  the  disease.  There  were  no  cases 
seen  of  what  might  be  regarded  as  the  abortive  form  of  the 
disease.  Cases  of  this  have  been  reported  in  early  epidemics 
in  which  patients  would  be  suddenly  attacked  with  the  phe- 
nomena of  the  disease  in  an  intense  form,  and  in  a  short  while, 
often  in  twenty-four  hours,  all  the  symptoms  would  disappear.* 
These  cases  were  most  frequently  seen  in  children,  and  occurred 

*  Such  cases  would  be  seen  more  likely  in  private  practice  than  in  hospitals. 


126 

in  the  course  of  severe  epidemics.  It  is  very  possible  that  in 
many  cases  these  sudden  symptoms  may  have  had  some  other 
origin,  and  only  the  presence  of  an  epidemic  caused  them  to 
be  referred  to  meningitis.  Until  the  diagnosis  in  these  cases 
shall  be  confirmed  by  spinal  puncture  they  must  always  remain 
in  doubt. 

We  can  distinguish  an  acute  type  which  will  include  the 
fulminating  type.  In  the  acute  should  be  reckoned  those  cases 
in  which  the  active  symptoms  last  not  more  than  fifteen  days. 
In  these  acute  cases  the  term  of  the  patient  in  the  hospital  is 
much  longer,  but  he  is  then  recovering  from  the  conditions  which 
the  disease  has  left.  In  the  fulminating  type  those  cases  should 
be  included  which  are  fatal  within  forty-eight  hours  from  the 
onset.  The  chronic  form  includes  those  cases  in  which  the 
symptoms  from  the  beginning  are  not  so  active,  and  in  which 
during  the  course  of  the  disease  there  are  remissions  and  exacer- 
bations. 

The  intermittent  form  is  founded  mainly,  on  the  character  of 
the  temperature.  In  this  there  may  be  complete  intermissions 
of  the  temperature  with  or  without  abatement  of  the  other  phenom- 
ena. It  would  seem  probable,  from  some  results  which  have 
been  obtained  from  spinal  puncture,  that  the  exacerbations  in 
this  type  correspond  to  multiplication  and  fresh  invasions  of 
the  organisms  causing  the  disease,  they  having  previously  been 
quiescent. 

Acute  Type,  including  Fulminating  Cases. 
The  very  acute  type  of  the  disease  appears  to  have  been  more 
common  in  the  early  epidemics  than  in  the  late.  In  Jackson's 
report  to  the  Massachusetts  Medical  Society^*^  he  says  many  of  the 
cases  died  suddenly  in  ten  to  twelve  hours,  others  in  twenty-four, 
thirty-six,  or  forty-eight  hours  after  the  first  symptoms.  Some 
physicians  who  had  much  experience  with  the  disease  considered 
the  patients  safe  if  they  passed  the  first  twenty-four  hours  without 
mortal  symptoms.  North^^  says  that  patients  may  die  in  the  first 
twelve  to  twenty-four  hours.     Woodward'^*^  says  death  often  ap- 


127 

peared  in  ten  to  twelve  hours  after  the  first  attack.  Lowy/^  in 
the  epidemic  in  Papa,  had  one  case  in  which  death  took  place  in 
twelve  hours  ;  in  another,  in  three  days. 

Frew"  gives  the  following  history  of  a  fulminating  case.  Girl, 
aged  eight  and  a  half  years,  in  good  health  up  to  the  evening  of 
February  28,  when  she  went  to  bed  complaining  of  headache. 
She  afterwards  arose  and  stood  by  the  fire  for  some  time,  and 
was  found  in  the  morning  at  4  a.m.,  almost  comatose.  She  com- 
plained of  thirst,  and  asked  for  water.  She  drank  greedily,  but 
vomited  it  immediately  afterwards,  mixed  with  greenish  matter. 
Previously  she  had  vomited  in  bed.  At  6  a.m.  she  got  out  of 
bed,  partially  unconscious,  and  walked  across  the  room  to  procure 
more  water,  which  she  immediately  vomited.  She  seemed  to  be 
shaking  all  over,  and  died  at  9  a.m. 

Giuliui'"  reports  such  a  case  in  a  child  five  and  a  half  years  old. 
At  5  P.M.  she  was  suddenly  attacked  with  pain  in  head,  weakness, 
pain  in  bones  and  chill ;  at  6  p.m.  vomiting  and  diarrhoea  came 
on,  which  continued  during  the  night,  together  with  great  rest- 
lessness, fever  and  thirst.  In  the  morning  at  6  o'clock  general 
convulsions  occurred,  varying  with  spasmodic  cramps  of  both 
upper  and  lower  extremities.  These  convulsive  movements  ap- 
peared whenever  the  skin  was  touched.  At  9.30  consciousness 
was  lost.  Urine  and  fgeces  were  passed  unconsciously.  Tem- 
perature of  skin  increased,  pulse  hardly  perceptible ;  abdomen 
retracted ;    death  took  place  shortly  afterwards. 

Haiiser'^  reports  a  case  in  which  death  took  place  five  hours 
after  the  initial  symptoms.  Many  of  Eichter's^^  cases  were  ful- 
minating, death  taking  place  in  twelve  to  fourteen  hours.  In 
Klarner's"  cases  death  took  place  in  one  in  ten  and  another  in 
twelve  hours. 

Bauer^*^  thinks  that  in  the  beginning  of  epidemics  these  very 
acute  cases  are  more  common  than  towards  the  end.  There  have 
been  very  few  post-mortem  examinations  on  these  fulminating 
cases  reported,  and  there  are  no  reports  of  microscopic  exami- 
nations. In  the  post-mortem  examinations  which  have  been 
made,  no  exudation  was  apparent  to  the  naked  eye.     There  was 


128 

intense  hyperaemia,  with  cloudiness  of  the  meninges.  In  an  au- 
topsy by  Haiiser  on  his  first  case,  which  died  in  six  hours,  there 
was  no  pus,  but  simply  cloudiness  of  the  meninges. 

That  extensive  lesions  both  in  the  meninges  and  brain  can  be 
produced  in  a  short  time  is  seen  in  the  case  of  experimental 
meningitis  in  a  goat.  The  duration  of  the  disease  in  this  case 
could  not  have  been  more  than  twelve  hours. 

Eight  of  our  cases  were  extremely  acute.  In  five  of  these  the 
time  from  onset  to  death  was  three  days,  in  one  two  days  and  in 
two  about  thirty-six  hours.  Certainly  in  one  of  these  cases  the 
history  seemed  to  have  been  at  fault,  for  at  the  autopsy  there  was 
extensive  diplococcus  pneumonia. 

Chronic  Type. 

The  chronic  form  has  been  seen  in  all  of  the  epidemics. 
Woodward'''^  says  that  some  patients  survive  the  acute  symptoms 
and  afterwards  die,  seeming  to  sink  away  under  the  load  of  the 
disease.  They  become  cold  and  die  comatose,  with  all  the  marks 
of  general  mortification.  ClozeP  gives  a  peculiar  case  of  the 
chronic  form.  A  soldier  was  carried  in  a  delirious  condition  into 
the  hospital  on  the  21st  of  May.  On  the  29th  all  the  symptoms 
of  excitation  had  disappeared.  The  patient  fell  into  a  coma  and 
remained  in  this  condition  for  two  months.  He  speaks  of  another 
case,  which  lasted  from  the  16th  of  February  until  the  6th  of  May. 
Daga^*  gives  a  typical  history  of  a  chronic  case  which  lasted  from 
the  19th  of  March  until  the  27th  of  May,  and  which  eventually 
recovered. 

Osier®*  reported  a  case  of  blindness  following  chronic  meningitis 
in  which  there  was  gradual  restoration  of  sight.  The  child  had  a 
typical  acute  attack  five  months  previously.  This  may  have  been 
the  remittent  form,  for  the  report  says  she  recovered  and  was 
sitting  up  in  bed,  then  had  a  second  attack  with  high  fever  and 
stiffness  of  the  extremities. 

Martin  and  Levall  (Daga")  give  an  admirable  account  of  this 
chronic  form.  They  say  that  there  is  as  much  danger  at  the  end 
as  at  the  beginning  of  the  disease.  Recovery  takes  place  with 
difficulty,  and  it  is  impossible  to  say  when  it  begins.     There  may 


129 

be  weakness  of  the  limbs,  paralysis  of  various  muscles,  and  after 
the  paralysis  disappears  the  limbs  may  remain  feeble. 

Long-continued  diseased  conditions  which  may  be  due  to  faulty 
enervation  are  not  uncommon.  The  wretched  patients  may  be 
reduced  to  skeletons.  The  skin  is  dry,  the  face  without 
expression,  they  lie  on  their  beds  heavily  covered,  silent, 
indifferent  to  what  is  taking  place  around  them.  They  answer 
with  difficulty  questions  addressed  to  them.  They  have  no 
appetite  for  food,  and  the  stomach  often  rejects  the  food  which  is 
taken.  The  temperature  is  diminished  (in  one  case  Daga  saw 
it  descend  to  34^°  C),  the  marasmus  continues,  and  they 
eventually   die. 

Leyden®  says  that  if  the  first  attack  does  not  kill  there  may  be 
a  return  of  the  process,  and  the  patients  may  eventually  die  in  the 
long  convalescence. 

The  cases  reported  by  Hart^  in  Birmingham  seem  nearly  all  to 
have  been  of  the  chronic  form.  The  shortest  case  lasted  three 
weeks,  the  longest  fourteen  weeks.  In  the  long-standing  cases 
there  was  great  emaciation.  In  thirteen  of  the  fatal  cases  in  this 
epidemic  the  average  duration  of  the  disease  was  forty-three  days. 
In  one  case,  in  which  a  post-mortem  examination  was  made,  the 
duration  was  seventy-four  days,  and  in  another  the  time  given  was 
thirty  days,  and  may  have  been  much  longer.  In  two  of  the  cases 
which  recovered,  and  in  which  the  disease  ran  a  typical  chronic 
course,  with  numerous  complications,  remissions  and  exacerba- 
tions, the  duration  was  five  months.  The  cases  described  by 
Hirsch^  as  the  typhoid  form  come  under  the  chronic  type. 

The  symptoms  in  these  chronic  cases  may  be  due  to  the 
persistence  of  conditions  left  by  the  acute  attack.  The  exudation 
may  not  be  absorbed  completely  and  a  slow  form  of  inflammation 
may  be  developed.  It  is  probable  also  that  an  extensive  and 
general   neuritis   may   follow. 

The     iNTERJVnXTENT    AND     REMITTENT     TtPES. 

These  types  are  common.  The  disease  is  characterized  by 
decided  remissions,  or  in  some  cases  actual  intermissions,  in 
which  not  only  the  fever  but  all  of  the  other  symptoms  of  the 


130 

disease  abate.  The  remissions  may  be  followed  by  exacerbation 
of  all  the  symptoms.  These  cases  are  probably  due  either  to  the 
successive  involvement  of  parts  of  the  meninges  which  have  been 
hitherto  free  from  inflammation  or  to  a  fresh  growth  of  the 
organisms.  A  case  seen  at  the  Children's  Hospital  would  point  to 
this.  In  this  case  two  spinal  punctures  made  at  periods  of 
remission  showed  an  almost  clear  fluid,  with  absence  of  organisms 
microscopically  or  in  culture.  A  spinal  puncture  made  during  one 
of  the  exacei-bations  gave  a  cloudy  fluid,  containing  numerous  pus 
cells  and  diplococci.  In  the  present  epidemic  there  have  been 
numerous  cases  of  this  form.  Cases  11,  50,  70,  72  and  108, 
with  temperature  charts,  show  the  characteristics  of  this  form. 
Leyden®-  gives  a  case  which  was  marked  by  complete  intermission 
of  all  symptoms.  Child  aged  sixteen  years  was  taken  ill  on  the 
19th  of  April  with  headache,  pain  in  the  neck  and  vomiting.  On 
the  24th  of  April  she  returned  to  school,  and  remained  well  until 
May  1.  She  was  again  taken  with  vomiting  and  intense  pain  in 
the  head.  From  the  7th  to  the  11th  of  May  she  was  again  in 
school.  On  the  11th  there  was  a  chill,  headache,  intense  pain  in 
the  neck,  piercing  pain  in  the  eyes,  continued  vomiting  and 
delirium.  Throughout  this  attack  vomiting  was  seen  to  be  one  of 
the  most  dangerous  symptoms,  as  it  prevented  the  patient  from 
taking  any  nourishment.  There  was  slow  recovery  by  June  19. 
Lowy  saw  one  case  in  which  there  was  a  relapse  three  weeks  after 
the  disease  was  apparently  recovered  from.  The  second  attack 
began  with  vomiting,  intense  headache,  etc.,  just  as  the  first 
attack  did.  Meschede™  reports  a  case  which  showed  an  intermit- 
tent type  during  the  fourteen  weeks  of  the  disease.  It  began 
with  chills,  vomiting,  painful  stiffness  of  the  neck  and  neuralgic 
pains.  Henoch'^  speaks  of  the  frequent  intermittent  course  of  the 
disease.  Most  of  his  cases  were  in  children.  The  disease  began 
with  the  usual  acute  symptoms,  then  the  fever  diminished  and  the 
symptoms  disappeared.  After  a  short  interval  of  twenty-four 
hours  or  several  days  all  of  the  symptoms  again  appeared  and  the 
general  condition  became  worse.  In  these  cases  there  was  a 
general  absence  of  the  phenomena  which  point  to  the  involvement 
of  the  spinal  cord. 


131 


SYMPTOMS. 

Wunderlich^*'  divides  the  symptoms  of  the  disease  into  two 
groups :  in  the  first  group,  he  includes  those  which  depend 
upon  the  local  disturbances  of  the  cerebro-spinal  organs ;  and  in 
the  second,  those  which  must  be  regarded  as  evidence  of  a  general 
disturbance  of  the  organism.  Among  the  constitutional  symptoms 
he  speaks  of  the  enlargement  of  the  spleen,  the  eruption  of  the 
skin,  haemorrhages,  and  secondary  inflammations,  especially  of 
the  lungs.  In  the  most  severe  and  rapidly  fatal  cases  the 
symptoms  of  both  groups  seemed  to  be  united.  In  the  least 
severe  cases  the  nervous  symptoms  are  more  predominant  and  are 
more  important  for  diagnosis. 

Berg"  divides  the  symptoms  into  three  classes  :  — 

1.  Those  produced  by  the  poison  of  the  disease,  chills,  con- 
vulsions, fever,  vomiting,  nasal  catarrh,  constipation,  skin  erup- 
tions, emaciation  and  affections  of  the  joints. 

2.  Symptoms  produced  by  inflammation  of  the  cord,  stiffness 
of  the  neck,  opisthotonos,  pain  along  spine,  hemiplegia,  difficulty 
in  micturition,  incontinence  of  fjeces  and  urine. 

3.  Symptoms  produced  by  inflammation  of  the  brain,  headache, 
slow  pulse,  hydrocephalic  cry,  vertigo,  convulsions,  delirium, 
stupor,  coma  or  coma  vigil,  Cheyne-Stokes  respiration,  eye  symp- 
toms, ptosis,  strabismus,  internal  inflammation  of  the  eye,  con- 
junctivitis, corneitis,  paralysis,  hemiplegia  and  paraplegia. 

"We  have  not  made  any  attempt  at  such  a  classification  of  the 
symptoms  nor  is  it  possible  with  our  present  knowledge  to  do  so. 

Vomiting. 
Leyden®-  regards  vomiting  as  one  of  the  most  common  symptoms 
of  the  disease.  It  may  become  a  complication  which  seriously  in- 
terferes with  recovery.  In  one  of  the  cases  reported  by  Leyden 
there  was  constant  vomiting,  which  prevented  the  patient  from 
taking  food,  and  which  constituted  one  of  the  most  dangerous 
symptoms  of  the  case.  In  our  one  hundred  and  eleven  cases 
vomiting  was  absent  in  but  forty-one,  and  in  nearly  all  of  these 
stupor    and    unconsciousness    or   delirium  was  marked   from  the 


132 

beginning.  Vomiting  may  appear  among  the  initial  symptoms, 
or  later  in  the  course  of  the  disease.  It  is  generally  regarded 
as  cerebral  in  origin,  and  due  to  direct  or  reflex  stimulation  of  the 
vomiting  centre.^ 

Delirium. 

In  all  of  the  accounts  of  epidemics  which  we  have  gone  over 
delirium  is  mentioned  as  among  the  most  common  symptoms. 
North  says  that  violent  mania  may  come  on  in  a  few  hours  after 
the  onset,  especially  in  sanguine  young  men.  It  was  present  in 
sixty  of  the  cases  reported  by  us.  The  character  of  the  delirium 
varied  greatly,  sometimes  being  so  violent  that  the  patient  had  to 
be  forcibly  restrained  ;  in  other  patients  it  was  of  the  low  mutter- 
ing variety.  In  many  cases  it  developed  very  early,  and  in  others 
at  a  late  period  of  the  disease.  It  was  not  more  frequently  present 
in  the  cases  which  died  than  in  those  which  recovered.  Some 
patients  were  delirious  from  the  time  they  entered  the  hospital 
until  death ;  in  others  there  were  periods  of  delirium,  alternating 
with  periods  of  consciousness.  The  attacks  of  delirium  were  not 
always  coincident  with  increase  of  temperature  and  aggravation  of 
the  other  symptoms. 

Pain. 

Pain,  sometimes  limited  to  the  head,  sometimes  extending  all 
over  the  body  is  also  a  common  symptom  of  the  disease.  North 
says  that  in  the  acute  forms  of  the  disease  the  pain  is  often 
agonizing  ;  in  the  more  common  form  the  pain  in  the  head  and 
limbs  is  less  severe.  Fiske"'  gives  the  following  graphic  descrip- 
tion of  the  character  of  the  pain:  "In  some  cases  a  pain 
resembling  the  sensation  felt  from  the  sting  of  a  bee  extends 
from  the  extremities  of  the  fingers  or  toes,  it  darts  from  the 
foot  or  hand  to  some  other  part  of  the  limbs.  After  traversing 
the  extremities,  generally  on  one  side  only,  it  seizes  the  head 
and  flies  with  the  rapidity  and  sensation  of  electricity  over  the 
whole  body,  occasioning  blindness,  fainting,  nausea,  with  inde- 
scribable distress  about  the  precordia." 

Almost  all  the  patients  in  the  epidemic  reported  by  Gahlberg-'' 
complained  of  severe  pain  in  the  head.     The  pain  was  so  severe 


133 

that  the  patients  often  tore  the  hair  or  struck  the  head  against 
the  wall.  The  pain  often  showed  an  intermittent  character, 
coming  on  from  day  to  day  at  the  same  time. 

Levy*'"  says  that  hypersesthesia  of  the  skin  was  constant  in  his 
cases,  and  could  be  made  out  even  in  a  comatose  condition  of 
the  patients.  It  might  extend  over  the  entire  body,  or  it 
might  affect  only  certain  portions.  The  patients  begged  not  to 
be  touched.  There  was  often  spasm  of  the  muscles  of  the  skin. 
Almost  without  exception  pain  was  a  constant  phenomenon  in 
the  cases  observed  in  this  epidemic.  The  headache  was  often 
agonizing,  and  was  felt  either  generally  or  to  a  greater  degree 
in  certain  portions  of  the  head.  Patients  often  complained  of 
headache  in  the  occipital  region,  extending  down  the  back ; 
in  other  cases  the  headache  was  frontal,  and  often  assumed 
the  character  of  an  intense  neuralgia.  In  a  few  cases,  mostly 
in  children,  the  first  symptoms  of  the  disease  were  colicky  pains 
in  the  abdomen,  and  in  some  cases  pains  in  the  extremities. 
Patients  often  buried  the  head  in  the  pillow  to  shut  out  light 
and  sound.  In  the  course  of  the  disease  the  pain  varied  in 
character  and  intensity.  There  were  periods  in  which  the 
patient  was  free  from  pain,  alternating  with  periods  in  which 
the  pain  would  become  more  intense.  These  severe  attacks  of 
pain  were  often  followed  by  periods  of  unconsciousness.  Pain 
was  more  constant  in  the  head  than  in  any  other  part.  The 
pain  suffered  can  easily  be  accounted  for.  The  general  pain 
in  the  head  is  due  to  the  inflammation  of  the  meninges.  The 
neuralgic  character  of  the  pain  may  in  some  instances  be  referred 
to  the  extension  of  the  process  from  the  meninges  to  the  Gasse- 
rian  Ganglia ;  the  pain  in  the  cervical  region  and  back  may 
be  referred  to  pressure  exerted  by  the  exudation  on  or  inflam- 
mation of    the  posterior  nerve  roots. 

Neck  Symptoms. 
Symptoms  referred  to  the  neck  were  found  in  all  but  twenty- 
eight  cases.     In  many  cases  there  was  pain  in  the  neck,  with  or 
without   pressure.      In   many  there   was    simple    stiffness   in  the 
muscles,  without  contraction  or   retraction   of   the   head.     In  all 


134 

these  cases  any  attempts  to  move  the  head  or  neck  increased 
the  pain.  The  muscle  contractions  were  sometimes  limited  to  the 
neck ;  in  some  cases  the  muscles  of  the  back  were  also  affected, 
producing  opisthotonos.  In  one  case  in  which  the  neck  symptoms 
were  absent  the  post-mortem  examination  showed  that  the  cervical 
cord  was  very  slightly  affected.  It  is  obvious  that  all  these 
symptoms  can  be  referred  to  the  effect  of  pressure  on  or  inflamma- 
tion of  the  spinal  nerve  roots. 

Coma,  etc. 
Various  disturbances  of  consciousness,  which  varied  from  stupor 
and  drowsiness  to  deep  coma,  were  noted.  In  some  cases  coma 
came  on  in  the  beginning,  and  the  patients  remained  in  a  comatose 
condition  until  death ;  in  other  cases  it  was  among  the  later 
symptoms.  StriimpeP^^  finds  the  same  variations  in  the  cerebral 
symptoms  a  in  the  temperature.  Variations  may  appear  not 
only  from  day  to  day  but  from  hour  to  hour.  Insensibility  will 
suddenly  give  place  to  consciousness,  intense  pain  in  the  head  may 
cease,  and  a  marked  opisthotonos  may  suddenly  relax. 

Paralysis. 

Paralysis  is  not  uncommonly  observed.  It  may  develop  during 
the  disease  and  disappear  shortly,  or  it  may  persist  for  some  time. 
We  have  not  found  any  cases  recorded  in  which  the  paralysis  was 
permanent. 

Gahlberg^  reports  paralysis  of  the  bladder  in  one  case  ;  in 
another,  paralysis  of  the  right  side  of  the  face  and  of  the  right 
upper  and  lower  extremity.  In  one  case  there  was  paresis  of 
the  tongue,  which  disappeared  in  eight  weeks  after  recovery. 
Mosler^'  reports,  in  one  case  which  recovered,  paresis  of  the 
lower  extremities.  Baxa-  found  that  the  disease  was  often 
accompanied  and  sometimes  followed  by  paralysis.  In  three 
out  of  twenty-nine  cases  reported  by  Leichtenstern*^"^  there  was 
complete  hemiplegia,  including  the  facial  nerve,  and  in  one  case 
paralysis  of  all  the  extremities,  including  the  rectum  and  blad- 
der.     In  one  of  Ziemmsen's  cases,   reported  by  Sittman,  there 


135 

were  left  hemiplegia  and  facial  paralysis  which  passed  off  in  a 
few  days  after  recovery.  Striirapel  observed  in  one  case 
unilateral  facial  paralysis ;  in  another,  well-marked  paralysis  of 
the  lower  extremities,  and  in  this  case  the  cerebral  symptoms 
were  not  so  marked  as  the  spinal.  In  our  cases  paralysis  was 
rare.  In  two  cases  there  was  unilateral  facial  paralysis ;  in 
one,  bilateral ;  in  one  paralysis  of  the  right  leg  ;  and  in  two, 
complete  hemiplegia.  In  one  of  the  cases  of  hemiplegia  in 
which  a  post-mortem  examination  was  made  the  exudation  in 
the  meninges  was  much  more  abundant  on  the  side  opposite 
the  paralyzed  side,  and  there  was  marked  purulent  infiltration  of 
the  cortex.  Minute  foci  of  haemorrhage  with  surrounding  puru- 
lent infiltration  were  found  in  the  internal  capsule. 

SKIX. 

Lesions  of  the  skin  seem  to  have  played  a  greater  part  in  the 
descriptions  of  the  early  epidemics  than  in  the  more  recent.  In 
the  early  epidemics  these  lesions  gave  the  commonly  accepted 
name  of  spotted  fever  to  the  disease.  Jackson  says  the  skin 
lesions  may  occur  in  any  stage  of  the  disease.  A  rash  or  miliary 
eruption  may  appear.  This  may  itch  and  the  skin  be  torn  by 
scratching,  resulting  in  the  formation  of  ulcers.  He  describes 
particularly  the  appearance  of  large  blisters,  often  from  two  to 
five  inches  in  length,  which  seem  to  have  been  more  common  in 
the  reports  of  the  disease  from  "Worcester  than  elsewhere 
(Woodward™) .  It  is  more  than  probable  that  these  large  blisters 
were  due  rather  to  the  treatment  than  to  the  disease.  Sweating 
was  induced  by  placing  billets  of  wood,  which  had  been  immersed 
in  boiling  water,  in  bed  with  the  patient.  Such  a  billet  of  wood 
in  bed  with  an  unconscious  patient  is  capable  of  producing  such 
blisters  very  easily.  Every  one  is  acquainted  with  similar  con- 
ditions which  have  been  produced  by  hot  water  bottles. 

The  frequency  of  the  skin  affections  in  the  first  epidemics 
varied  much,  according  to  the  different  observers.  One  found 
that  in  eighty  cases  only  four  had  any  affection  of  the  skin. 
Another  estimates  them  as  appearing  in  one-half  of  all  his  cases. 


136 

Jackson  did  not  regard  these  lesions  of  the  skin  as  the  seat  of  the 
disease,  but  as  being  merely  symptomatic. 

Vieusseaux  does  not  mention  these  lesions  of  the  skin.  North 
gives  a  very  good  description  of  the  eruption.  He  says  "they 
take  the  form  of  blind  haemorrhages,  where  the  blood  flowing  from 
the  vessels  of  the  skin  is  detained  beneath  the  cuticle,  forming 
petechial  spots.  So  frequent  was  this  species  of  haemorrhage  in 
the  early  part  of  the  epidemic  that  it  was  considered  one  of  the 
most  striking  characteristics,  and  gave  rise  to  the  name  petechial 
or  spotted  fever,  which  has  been  very  generally  but  inaccurately 
given  to  the  disease.  These  spots  appear  commonly  on  the  face, 
neck  and  extremities,  frequently  over  the  whole  body.  They  were 
generally  observed  in  the  early  stages  of  the  disease ;  in  size  the 
head  of  a  pin,  and  a  six-cent  piece  would  mark  the  two  extremes. 
They  were  evidently  formed  of  extraversated  blood.  They  do  not 
arise  above  the  surface  and  do  not  recede  upon  pressure.  In 
color  they  vary  from  a  common  to  a  very  dark  purple,  and  the 
darker  the  shade  the  more  fatal  the  prognosis.  These  spots, 
which  in  1806-1807  marked  almost  every  case,  in  1808-1809  were 
rarely  observed." 

Woodward'^^  says  there  was  soreness  of  the  flesh,  and  spots 
appeared  on  the  skin  the  size  of  half  a  common  duck  shot, 
resembling  blood  blisters. 

North,  in  a  letter  to  the  Philadelphia  Medical  Museum,  says 
further  that  some  of  the  patients  have  in  the  true  skin  spots  which 
resemble  flea  bites.  One  patient  was  covered  all  over  with  such 
spots  for  a  number  of  days,  but  more  commonly  there  were  a  few 
scattered  ones  on  different  parts  of  the  body.  They  are  of 
different  grades  of  color,  from  red  to  dark,  some  resembling 
bruises.  Fiske  says  an  eruption  of  the  skin  is  not  a  constant 
attendant  on  the  disease.  It  generally  comes  on  in  some  form  or 
other,  according  to  the  violence  of  the  disorder ;  sometimes 
appearing  as  a  miliary  eruption  over  the  entire  body.  It  may 
appear  in  patches  in  the  bend  of  the  arm  or  the  breast  or  neck, 
without  any  discoloration  at  first.  These  skin  eruptions  seem  to 
have  been  especially  abundant  in  the  epidemics  in  Ireland  in  1866 
and  1867 . 


137 

Gordoa^"^  observed  ia  one  case  an  eruption  something  like 
measles,  but  the  patches  were  irregular  in  size  and  shape.  They 
were  dark  colored,  rough  looking  on  the  surface  and  thickly 
interspersed  with  petechias.  In  another  place  he  describes  a 
definite  eruption,  which  conies  out  with  great  rapidity  and  is 
found  on  all  parts  of  the  body,  but  chiefly  on  the  lower  extrem- 
ities. It  is  of  a  very  dark  color,  sometimes  deep  brown  or 
purple,  or  even  black.  In  some  cases  it  is  studded  with  black 
spots,  appearing  on  the  nose  or  face  of  the  patient  as  though 
a  quantity  of  black  ink  were  scattered  over  his  face. 

Marston  found  in  very  few  cases  an  intense  eruption  of 
petechiee,  which  was  followed  by  rapid  coma  and  collapse.  The 
rapidity  with  which  this  very  dark  eruption  appeared,  its  great 
extension  and  the  deep  collapse  which  accompanied  it  gave  to 
the  cases  a  frightful  appearance,  and  caused  the  people  to  describe 
it  as  the  black  death. 

In  all  of  the  investigations  on  this  epidemic  in  Ireland  it 
was  seen  that  the  nervous  symptoms  preceded  the  affection  of 
the  skin  even  in  the  most  rapid  cases. 

In  Upham's  cases,  in  Newbern,  petechias  often  identical  with 
those  of  true  typhus  were  seen  in  all  parts  of  the  body  except 
the  face. 

In  the  epidemic  reported  by  Hermann  and  Kober^  petechise  on 
the  skin  or  conjunctiva  were  frequently  seen.  Many  of  the 
cases  reported  by  Richter^^  had  petechise  and  ecchymoses. 
Gahlberg  says  that  the  skin  eruptions  may  vary,  and  he  has 
seen  one  case  in  which  it  was  ver}^  similar  to  measles.  In  the 
report  by  Tipton"^  purpuric  spots  occurred  in  some  cases,  but 
they  were  generally  absent. 

Herpes  is  far  more  common  than  any  other  form  of  eruption. 
It  is  more  common  on  the  lips  and  nose,  but  may  appear  on 
other  parts  of  the  face  and  even  elsewhere  on  the  body. 

Klemperer'''  speaks  of  the  frequency  of  herpes  in  meningitis, 
and  says  it  is  more  common  in  the  epidemic  than  in  any  other 
form. 

Leichtenstern  found  herpes  in  twenty-six  out  of  twenty-nine 
cases  examined. 


138 

Frey^  describes  herpes  as  very  common  in  the  epidemic  re- 
ported by  him. 

Hallenstein  says  that  herpes  is  the  most  common  of  the  skin 
affections  of  the  disease.  It  is  most  common  on  the  nose  and 
mouth,  then  on  the  cheek,  forehead,  eyes  and  ears.  More 
rarely  there  is  an  eruption  of  the  vesicles  on  the  neck  and  ex- 
tremities. RoUet^^®  did  not  find  herpes  common  in  the  cases 
examined  by  him,  although  he  says  it  was  present  in  Strassburg 
in  nearly  all  the  cases.  Friis  in  the  epidemic  in  Copenhagen 
found  herpes  of  the  lips  in  seventeen  cases.  Decloux^^  found 
herpes  and  other  skin  eruptions  in  all  of  the  cases  which  recovered. 

In  this  series  of  one  hundred  and  eleven  cases  herpes  was 
mentioned  as  occurring  in  thirty-five  cases.  It  is  possible  that 
its  presence  was  not  always  noted.  The  amount  of  it  varied 
from  an  eruption  of  a  few  fine  vesicles  to  an  abundant  eruption 
of  large  vesicles.  Cultures  were  not  made  from  the  contents 
of  the  vesicles. 

Petechise  or  larger  hsemorrhagic  foci  in  the  skin  were  found 
in  eleven  eases.  They  were  most  abundant  in  two  fatal  cases, 
the  duration  in  one  case  being  two  days,  in  the  other  seven 
days.  In  the  two-day  case,  that  Of  a  child,  there  was  present 
all  over  the  body  an  abundant  eruption,  which  developed  with 
great  rapidity.  The  spots  were  more  commonly  found  over  the 
elbows  and  knees.  Circumscribed  areas  of  hypersemia  which  dis- 
appeared on  pressure  were  mentioned  in  a  few  cases.  Hgemor- 
rhages  in  the  skin  were  found  in  but  one  of  the  cases  in  which 
a  post-mortem  examination  was  made.  In  the  centres  of  some 
of  these  there  was  a  beginning  formation  of  pustules. 

PNEUMONIA. 

The  relation  between  pneumonia  and  the  epidemic  meningitis 
has  been  complicated  by  confusing  other  forms  of  meningitis  with 
this.  Meningitis  is  sometimes  seen  in  connection  with  acute 
croupous  pneumonia,  and  is  due  to  a  metastasis  from  the  lungs. 
And  from  this  it  has  become  a  common  belief  that  pneumonia 
is  a  frequent  complication  even  of  epidemic  meningitis.     In  most 


139 

cases  the  character  of   the   pneumonia   is   not   defined,  but  it  is 
apparent  that  croupous  pneumonia  is  referred  to. 

It  has  been  frequently  stated  that  epidemics  of  pneumonia 
have  occurred  at  the  same  time  with  epidemics  of  cerebro-spinal 
meningitis,  and  this  statement  has  been  used  by  those  who 
sought  in  the  pneumococcus  the  cause  of  epidemic  meningitis. 
We  have  not  been  able  to  find  the  authority  for  such  a  state- 
ment. It  is  very  possible  that  the  opinion  of  the  relation 
between  the  two  may  be  due  to  the  fact  that  both  diseases  are 
more  common  at  the  same  time,  —  that  is,  in  the  late  winter 
and  spring.  Practically  all  of  these  accounts  of  the  relation 
between  the  two  diseases  come  from  clinical  sources. 

Levy^  remarks  on  the  frequency  with  which  congestion  of 
the  lungs  is  found  as  a  complication.  He  thinks  this  condition  is 
rather  a  consequence  than  a  complication  of  the  disease,  and  is 
due  to  the  hebitude  of   the  patient  and  the  dorsal  decubitus. 

Jaffe^*^'',  who  reported  the  epidemic  in  Hamburg,  found  but  one 
case  of  typical  fibrinous  pneumonia  with  meningitis,  and  the 
clinical  history  of  this  case  would  rather  show  that  the 
meningitis  followed  the  pneumonia  and  was  probably  due  to 
the  pneumococcus. 

Immerman  and  Heller*^  speak  of  the  frequency  of  complica- 
tions of  croupous  pneumonia  with  purulent  meningitis  at  the 
close  of  the  epidemic  in  Erlangen  in  1866.  They  say  that  after 
a  pause  of  several  months,  from  August,  1866,  up  to  January, 
1868,  thirty  cases  of  pneumonia  were  seen,  nine  of  which  were 
complicated  with  meningitis.  This  appeared  at  the  end  of  the 
epidemic,  and  they  think  there  is  no  relation  between  the  two, 
but  that  the  epidemic  meningitis  paves  the  way  for  the  pneu- 
monia. 

Leichtenstern,  in  his  admirable  account  of  the  epidemic  in 
Cologne,  takes  up  the  question,  and  does  not  believe  that  there 
is  any  relation  between  the  two. 

Croupous  pneumonia  was  found  at  the  post-mortem  examina- 
tions of  two  of  our  cases.  In  these  the  pneumonia  was  the  result 
of  infection  with  the  pneumococcus  which  was  found  in  the  lungs, 
while  the  diplococcus  intracellularis  was  found  in  the  lesions  in  the 


140 

brain.  In  several  of  our  cases  there  were  small  foci  of  broncho- 
pneumonia and  small  areas  of  congestion  in  the  lungs  from  which 
the  pneumococcus  along  with  other  organisms  was  obtained. 

It  is  very  possible  that  many  of  the  cases  of  pneumonia  which 
have  been  reported  in  connection  with  epidemic  meningitis  were 
not  cases  of  genuine  croupous  pneumonia,  but  cases  of  diplo- 
coccus  pneumonia.  This  was  found  in  eight  cases  and  in  one 
the  amount  of  lung  involved  was  so  extensive  that  it  could  have 
been  mistaken  both  clinically  and  anatomically  for  a  case  of 
croupous  pneumonia.  Leichtenstern  found  no  cases  of  croupous 
pneumonia  in  the  epidemic  reported  by  him,  and  opposes  the 
prevalent  view  that  the  pneumococcus  is  the  cause  of  epidemic 
meningitis.  He  says  "  pneumonia  is  a  disease  spread  over  the 
entire  earth,  and  appears  at  all  times,  there  being  no  land 
immune  from  it.  Epidemic  meningitis  is  very  rare,  and  in  many 
countries  is  still  unknown.  Croupous  pneumonia  attacks  every 
age,  the  disposition  increasing  somewhat  with  increasing  age. 
Epidemic  meningitis  is  a  disease  which  affects  children  and 
young  people ;  beyond  thirty-five  there  is  slight  disposition 
towards  it.  Croupous  pneumonia  has  a  typical  course  and  a 
crisis  ;  epidemic  meningitis  has  no  crisis.  The  complications  of 
the  two  diseases  are  different.  Epidemic  meningitis  frequently 
shows  multiple  synovitis  as  a  complication ;  this  is  extraordi- 
narily rare  in  croupous  pneumonia.  The  affections  of  the  eye, 
etc.,  which  are  seen  in  meningitis,  are  extremely  rare  in  pneu- 
monia. The  character  of  the  exudation  in  the  two  diseases  is 
different,  being  more  fibrinous  in  croupous  pneumonia.  It  is 
often  difficult  to  make  a  differential  diagnosis  between  menin- 
gitis and  severe  pneumonia  with  predominant  brain  symptoms." 

In  these  cases,  according  to  Leichtenstern,  at  the  time  of  the 
crisis,  the  brain  symptoms  drop  just  as  the  other  symptoms.  He 
thinks  it  is  also  possible  to  distinguish  clinically  between  menin- 
gitis arising  as  a  complication  of  pneumonia  and  epidemic 
meningitis.  In  meningitis  following  pneumonia  contraction  of  the 
muscles  of  the  neck  is  often  absent,  while  in  epidemic  meningitis 
it  is  almo'st  invariably  present.  Pneumonia-meningitis  soon  leads 
to  delirium  and  coma,  while  in  the  epidemic  form  the  sensorium 


141 

may  be  normal  throughout  the  entire  course.  Pneumonia- 
meningitis,  moreover,  is  rapidly  fatal,  while  the  epidemic  form  is 
frequently  recovered  from.  The  remissions  and  exacerbations, 
the  varying  course  and  relapses,  the  following  hydrocephalus,  the 
uncertain  gait,  the  eye  and  ear  affections, — are  all  exclusive 
attributes  of  the  epidemic  form. 

Runeberg^^  reports  a  case  of  pneumonia  with  following  menin- 
gitis which  recovered,  but  in  this  case  the  symptoms  of  meningitis 
were  not  definite.  In  one  of  Weichselbaum's  cases  there  was 
lobar  pneumonia  in  connection  with  the  meningitis.  He  found  the 
pneumococcus  in  the  lobar  pneumonia  and  the  diplococcus  in  the 
meninges. 

Striimpel  does  not  mention  croupous  pneumonia  as  a  complica- 
tion in  his  cases. 

THE    EYES. 

Symptoms  relating  to  the  eyes  have  a  prominent  place  in  the 
descriptions  of  epidemics  of  meningitis.  North  describes  dila- 
tation and  in  some  cases  contraction  of  the  pupils,  redness  and 
suffusion  of  the  conjunctiva,  double  or  triple  vision,  and  in  a 
few  cases  there  was  total  blindness.  Woodward  says  that  the* 
eyes  are  red  and  watery.  The  pupils  are  dilated  in  some  cases, 
in  others  they  are  small,  like  those  of  dying  persons.  Bestor'^® 
says  the  eyes  are  often  red  and  suffused,  and  the  pupils  are 
enlarged.  There  may  be  double  or  triple  vision,  and  in  some 
cases  there  was  partial  or  total  blindness  after  the  first  twenty- 
four  hours.  Baxa-  says  blindness  is  often  seen  in  cases  which 
recover.  Friis-^  examined  the  eyes  in  thirteen  out  of  thirty 
cases,  and  in  three  of  these  cases  he  found  congestion  of  the 
optic  papilla.  Tourdes^^'  found  ophthalmia  in  six  of  his  cases  ; 
in  three  cases  it  occurred  during  convalescence,  and  was  not 
severe.  Daga,^^  in  the  epidemic  in  Metz,  found  purulent  oph- 
thalmia in  a  number  of  cases,  but  he  considers  this  to  be  an 
accidental  complication  which  is  not  usually  dangerous.  Wilson^^ 
says  the  eyelids  may  be  enormously  swollen,  and  present  the 
appearance  of  purulent  ophthalmia  or  suppurative  inflammation 
of  the  eye-ball.     He  thinks  this  may  result  from  lack  of  sensa- 


142 

tion  and  exposure  of  the  eye.  The  anterior  chamber  often 
contains  pus  and  the  choroid  and  iris  are  often  affected. 
Blindness  may  occur  either  as  the  result  of  clouding  of  the  lens, 
with  adhesions  and  infiltration  of  the  iris,  or  of  atrophy  of  the 
optic  nerves.  Knapp^*^  found  eye  symptoms  in  four  or  five  per 
cent,  in  all  cases  of  meningitis.  They  appeared  ordinarily  during 
the  second  or  third  week  of  the  disease.  The  eye  symptoms 
often  took  the  form  of  more  or  less  intense  choroido-iritis,  which 
could  lead  to  blindness  in  three  or  four  days.  This  condition 
was  often  accompanied  by  injection  of  the  conjunctivae  and 
infiltration  of  the  cornea,  with  adhesions  and  discoloration. 
There  was  complete  blindness  in  ten  of  the  cases  observed  by 
Mm.  He  does  not  think  that  the  eye  lesions  can  be  regarded 
as  an  extension  of  the  inflammation  from  the  meninges  along  the 
optic  nerves,  but  regards  it  as  an  acute  idiopathic  iritis. 
Collins^^  observed,  relatively  frequently,  serious  affections  of  the 
eyes,  among  which  he  especially  speaks  of  irido-choroiditis  with 
separation  of  the  retina,  purulent  infiltration  of  the  eye  and 
atrophy.  Hirsch  describes  conjunctivitis  as  an  almost  constant 
symptom. 

In  the  epidemic  reported  by  Frey^  there  was  injection  of  the 
conjunctiva,  strabismus,  turgescence  of  the  eyeball  and  more  or 
less  serious  disturbances  of  sight. 

In  the  epidemic  described  by  Bllimm*  both  subjective  and 
objective  eye  symptoms  were  prominent.  The  patients  com- 
plained of  light.  In  one  case  there  was  destruction  of  the  cornea. 
He  thinks  that  softening  of  the  cornea  may  be  due  to  tropho- 
neurosis. 

Hallenstein^^  says  the  most  frequent  lesion  of  the  eye  is 
paralysis  of  the  oculo-motor  nerves,  producing  dilatation  of  the 
pupil,  divergent  strabismus  and  ptosis.  Next  to  this  comes 
paralysis  of  the  abducens  with  convergent  strabismus.  The  con- 
junctiva at  the  height  of  the  disease  is  injected,  reddened  and 
swollen.  There  are  also  affections  of  the  cornea,  appearing  as 
clouding  and  ulceration,  paralysis  and  spasms  of  the  eye  muscles, 
abnormal  narrowness  or  dilatation  of  the  pupils,  and  even  com- 
plete blindness.     The  blindness  may  result  either  from  a  purulent 


143 

inflammation  of  the  eye  with  separation  of  the  retina  and 
destruction  of  the  bulb,  or  from  an  optic  neuritis. 

Niemeyer^™  thinks  that  the  affections  of  the  eye  arise  from 
imperfect  nutrition  of  the  tissue,  due  to  inflammation  of  the 
trigeminus.  He  founds  his  views  on  the  fact  that  in  meningitis 
the  same  conditions  of  the  eye  are  seen  which  come  from  the 
destruction  of   the   Gasserian   ganglion. 

Rudnew  concludes  that  inflammation  of  the  eyes  is  not  sec- 
ondary to  the  meningitis,  and  does  not  arise  by  an  extension  of 
the  process  from  the  membranes  of  the  brain  to  the  eye.  It 
comes  simultaneously  with  the  affection  of  the  meninges,  and  is 
due  to  the  same  cause.  Disturbances  of  innervation  of  the  eye 
were  seen  in  almost  all  of  Striimpel's  cases.  He  says  the 
ophthalmoscopic  investigation  of  the  eye  may  show  changes 
without  the  sick  person  being  aware  of  any  disturbance  of  sight. 

Randolph*^,  in  the  epidemic  in  Lahaconing,  examined  the  eyes 
in  thirty-five  cases,  twenty  of  which  were  fatal.  He  reports  the 
different  cases  in  detail,  and  from  this  some  idea  of  the  character 
and  frequency  of  the  lesions  may  be  gained.  In  the  thirty-five 
cases  examined  the  fundus  was  normal  in  but  seven.  Of  these 
seven  cases  one  had  divergent  strabismus  and  dilated  pupils. 
The  right  eye  was  more  often  affected  than  the  left.  Every  case 
of  strabismus  was  of  the  divergent  variety.  He  found  congestion 
of  the  optic  disc  in  many  cases,  and  thinks  this  marks  the  begin- 
ning of  optic  neuritis.  There  was  atrophy  of  the  optic  nerves  in 
one  case  which  recovered.  Osler*^  has  reported  a  case  similar  to 
the  one  described  by  Jack  (page  144),  in  which  there  was  total 
blindness  following  a  case  of  meningitis  with  gradual  recovery  of 
sight  after  months.  Omerod''-  found  in  one  case  internal 
strabismus  of  the  right  eye,  but  the  fundus  of  each  was  normal. 
In  one  case  there  were  purpuric  spots  on  the  conjunctiva.  One  of 
the  cases  reported  by  Mills  and  CahalP  was  blind  and  deaf  three 
weeks  before  death.  In  the  cases  reported  by  us  no  systematic 
examination  of  the  eyes  was  made  in  all  cases. 

Various  abnormal  conditions  of  the  eyes  were  noted  in  sixty- 
seven  cases.  Strabismus,  usually  affecting  both  eyes,  was  noted 
in  twenty-eight  cases.     It  was  convergent  in  thirteen,  divergent 


144 

in  eight,  and  in  the  remainder  its  character  was  not  noted. 
Conjunctivitis  was  not  commonly  present ;  it  was  noted  in  but 
ten  cases,  and  in  these  the  condition  varied  from  injection  of 
the  conjunctiva  up  to  a  purulent  discharge.  In  one  case  the 
purulent  secretion  of  the  conjunctiva  was  examined  for  bacteria, 
but  no  diplococci  were  found.  In  many  cases  irregularity  in 
the  pupils  was  noted.  In  one  case  there  was  slight  bulging  of 
the  eyes.  No  post-mortem  examination  of  this  case  was  made, 
so  that  it  cannot  be  known  whether  this  condition  was  due  to 
purulent  infiltration  of  the  orbit.  Nystagmus  was  seen  in  but 
ten  cases.  In  none  of  the  cases  which  recovered  was  there 
complete  blindness. 

We  are  indebted  to  Dr.  Edwin  E.  Jack  for  the  following  de- 
scription of  the  eye  lesions  observed  by  him  in  the  cases  seen 
at  the  Children's  Hospital :  — 

The  conditions  found  were  conjunctivitis,  dessicating  keratitis,  stra- 
bismus, contraction  and  dilatation  of  the  pupil  with  little  or  no  reflex 
action,  inequality  of  pupils,  neuritis  of  various  grades,  from  redden- 
ing of  the  disc  to  violent  inflammation  of  the  choked-disc  variety,  post- 
neuritic atrophy  and  purulent  choroiditis.  No  cases  of  loss  of  vision 
without  ophthalmoscopic  appearances  such  as  might  occur  from  trouble 
at  the  convexity  were  observed,  though  one  case  in  which  no  ophthal- 
moscopic examination  was  made  must  remain  in  doubt.  Visual  aeute- 
ness  and  fields  of  vision  could  naturally  not  be  taken.  There  was  no 
implication  of  the  orbital  tissue  in  any  case  and  no  oedema  of  the  conjunc- 
tiva. Conjunctivitis  was  frequent.  The  dessicating  keratitis  seen  was 
due  to  the  imperfect  closure  of  the  lids  and  secondaiy  necrosis  of 
the  cornea.  Strabismus  caused  by  paralysis  or  irritation  of  the  ocular 
nerves  by  exudation  at  the  base  was  present  in  many  instances,  and 
in  those  personally  observed  was  always  convergent.  It  is  doubtful 
if  there  was  any  paralysis  of  the  third  nerve  except  so  far  as  the 
pupillary  branch  was  concerned.  Strabismus  seemed  to  have  no  con- 
nection with  the  severity,  length  or  outcome  of  the  disease.  Of  all 
the  children  still  alive  who  had  this  symptom  I  have  found  but  one 
in  whom  the  squint  persists,  though  diplopia  is  not  apparent.  No 
instances  of  conjugate  deviation  were  noted. 

Neuritis,  present  or  past,  as  shown  by  atrophy  of  post-neui'itic  character, 
was  present  in  at  least  six  cases,  and  probably  in  more ;  for,  in  addition 
to  the  cases  not  seen,  no  case  was  recorded  as  having  neuritis  without 
having  definite  signs  in  the  way  of  cloudiness  of  the  disc  or  distended  or 
tortuous  vessels.  It  was  suspected  in  others  from  the  appearances,  so 
that  the  number  is  probably  larger  than  stated.  It  is  often  hard,  even 
under  the  most  favorable  circumstances,  to  decide  whether  a  disc  is 


.      145 

abnormal  or  not;  but  in  these  children,  the  struggles  and  movements  of 
the  eyes  making  only  a  fleeting  glance  possible,  mucus  on  the  cornea  and 
in  some  instances  an  uneven  surface,  made  the  task  still  more  difficult. 
Neuritis  was  apparently  no  more  common  in  the  fatal  cases  than  in  those 
who  recovered,  and  was  most  marked  in  two  childi-en  who  still  live. 
One  of  these  had  violent  neuritis  with  htemorrhages,  which  had  not  then 
gone  on  to  atrophy,  and  the  sight  was  apparently  jDerfectly  good.  I  have 
recently  seen  this  child.  The  vision  is  as  good  as  ever,  the  discs  are 
normal,  showing  no  traces  whatever  of  the  previous  inflammation. 
The  other  is  a  remarkable  instance  of  restored  vision  after  weeks  of 
blindness.  The  child  was  ill  a  very  long  time,  was  extremely  emaciated 
and  had  decidedly  atrophic  discs.  Much  to  my  surprise,  two  weeks  ao-o 
I  found  a  vision  which  enabled  the  child  to  go  about  readily ;  the  disc 
was  more  pink  in  color  and  the  vessels  were  actually  larger.  Her 
mother  stated,  perhaps  with  exaggeration,  that  the  chikl  could  recoo-nize 
her  at  a  distance  from  the  yard  to  the  second  or  third  story  Avindow  In 
this  case  there  was  total  deafness,  which  has  persisted. 

There  were  two  eases  of  purulent  choroiditis.  This  condition  closely 
resembles  glioma  of  the  retina.  One  of  the  children  died,  the  other 
lived,  and  is  to-day  perfectly  well,  with  the  exception  of  a  useless  rio-ht 
eye.  The  fatal  case  was  a  very  marked  one,  with  a  historj-  of  some 
weeks'  illness  before  entrance.  It  was  said  by  the  parents  that  the  right 
eye,  meaning  probably  the  lids,  was  swollen  one  week  before,  and  that 
after  that  the  eye  began  to  look  small.  When  seen,  the  eye  was  much 
smaller  than  the  other,  soft,  had  considerable  ciliary  injection,  pupils  mod- 
erately dilated  (atropin  had  been  used),  iris  discolored,  its  pupillary  edo-es 
frayed  and  uneven,  and  from  behind  the  lens  was  seen  a  yellow  reflex 
tinged  with  red,  the  whole  making  a  typical  picture  of  what  is  known 
as  metastatic  choroiditis.  This  child  was  very  ill,  and  in  marked  con- 
trast with  the  other  one,  who  came  into  the  hospital  looking  perfectly 
well,  and  indeed  nothing  out  of  the  way  could  be  found.  The  day  pre- 
vious he  had  had  vomiting  and  slight  fever.  On  the  second  day  the  eyes 
were  looked  at  and  the  fundus  was  normal.  On  the  third  day  there  was 
vomiting,  jjallor,  coldness,  weak  pulse  and  the  child  seemed  partially 
unconscious,  but  was  better  in  the  evening.  Strabismus  was  apparent. 
Next  day  it  was  noticed  that  the  right  eye  was  red.  In  tAvo  or  three 
days  the  child  was  all  right  again,  the  strabismus  had  disappeared, 
and  from  that  time  he  seemed  well.  At  the  first  appearance  of  the  in- 
flammation in  the  eye,  on  account  of  great  difliculty  in  examination,  the 
child  screaming  loudly  even  when  approached,  nothing  was  made  out 
except  iritis  and  a  deposit  of  lymph  in  the  pupil.  Later  the  typical  yel- 
low reflex  was  visible,  making  the  diagnosis  cei"tain,the  general  apjjear- 
ance  resembling  that  already  described  in  the  first  ease,  though  the  eye 
was  not  so  shrunken  at  that  time. 

This  case  is  intei'esting  for  several  reasons :  first,  the  coincidence  in 
point  of  time  of  the  only  cerebral  symptoms,  and  the  beginning  of  the 
process  in  the  eye  ;  second,  the  fact  that  the  lumbar  jjuncture  was  neg- 
ative. With  reference  to  this,  on  account  of  the  possible  doubt  it  might 
throw  on  the  diagnosis,  it  should  be  stated  that  the  patient's  sister  died 


146     . 

at  this  same  time,  after  less  than  a  week's  illness,  of  undoubted  cerebro- 
spinal meningitis.  In  her  case  lumbar  jjuncture  was  positive  and  optic 
neuritis  was  present.  Third,  it  shows  that  this  complication  is  not 
limited  to  severe  or  fatal  cases. 

Notwithstanding  the  frequency  of  the  eye  complications  in 
cerebro-spinal  meningitis,  there  have  been  but  few  anatomical 
investigations  of  the  eyes  after  death.  Rudnew  and  Burzew 
examined  the  eye  in  one  case.  Pus  was  found  in  the  ciliary 
region  and  in  the  vitreous.  They  regarded  the  lesions  in  the 
eye  as  probably  embolic. 

Hoffman*^  reports  an  interesting  condition  of  the  eye  following 
meningitis.  There  was  complete  blindness  in  one  eye  in  a  case 
which  recovered,  with  ptosis,  dilated  pupils,  immobility  of  the 
eye-balls  and  swelling  of  the  lids.  This  condition  remained  for 
some  time.  He  then  operated,  and  found  the  sheath  of  the 
optic  nerves  dilated  into  an  ampular  form  and  evacuated  con- 
siderable pus. 

Saltini^^  investigated  the  eye  in  two  cases  of  meningitis.  One 
eye  was  removed  three  and  one-half  minutes  and  the  other  four 
or  five  minutes  after  death.  He  found  total  separation  of  the 
retina  and  extensive  inflammatory  destruction  especially  of  the 
anterior  equatorial  parts  of  the  uvea  and  retina.  There  was 
also  atrophy  of  the  optic  nerve,  with  cellular  infiltration  of  the 
sheath  and  of  the  septum. 

Leichtenstern  reports  that  at  one  autopsy  all  the  cranial 
nerves  were  bathed  in  the  exudation,  and  the  oculomotor  nerve 
was  rosy  red.  There  were  no  cases  seen  of  involvement  of  the 
optic  nerve,  and  no  cases  of  pan-ophthalmitis. 

Confusion  has  also  arisen,  in  that  this  form  of  meningitis 
has  not  been  distinguished  from  the  pneumococcus  and  other 
forms.  Axenfeld^  reports  four  cases  of  metastatic  inflammation 
of  the  eye,  due  to  the  pneumococcus,  and  two  of  these  were 
from  meningitis.  One  of  his  meningitis  cases  was  secondary 
to  an  acute  endocarditis.  He  found  no  continuity  between  the 
organisms  in  the  sheath  of  the  optic  nerve  and  those  in  the 
interior  of  the  eye.  There  were  fresh  capillary  emboli  in  the 
retina,  which  he  regarded  as  the  source  of  the  eye  lesions.     He 


147 

does  not  think  that  it  has  been  shown  in  a  single  undoubted 
case  that  there  is  a  continuity  between  the  inflammation  in  the 
eye  and  that  in  the  meninges.  In  one  of  the  autopsies  reported 
by  Klebs^^  there  was  purulent  infiltration  of  the  tissues  of  the 
orbit. 

When  we  review  the  eye  lesions  of  this  disease,  it  can  easily  be 
seen  that  they  are  due  to  three  causes.  In  the  first  place,  there 
may  be  neuritis  or  degeneration  of  the  nerves  of  the  eye,  due  to 
their  involvement  in  the  exudation  at  the  base  of  the  brain  without 
any  extension  of  the  inflammatory  process  to  either  the  orbit  or 
the  eye.  This  condition  seems  to  affect  the  oculomotor  more 
than  the  other  motor  nerves.  The  optic  nerves  may  also  be 
involved  in  this  exudation.  Secondly,  the  inflammation  from  the 
meninges  may  extend  directly  from  the  brain  into  the  eye,  the 
route  most  frequently  chosen  being  the  pia  arachnoid  of  this 
nerve.  All  of  the  cases  of  purulent  choroido-iritis,  and  the  very 
rare  cases  of  suppuration  in  the  orbit,  are  probably  due  to  such  an 
extension.  Most  of  the  ophthalmologists  seem  to  have  a  deeply 
rooted  belief  that  these  conditions  are  due  to  metastasis,  but  it  is 
plainly  not  a  metastasis  but  a  direct  extension.  Undoubtedly 
there  are  cases  of  metastatic  choroido-iritis  seen  in  connection 
with  other  forms  of  meningitis,  but  in  these  cases  both  the  menin- 
gitis and  the  eye  lesions  are  due  to  metastasis.  Such  are  the 
cases  of  meningitis  accompanying  acute  endocarditis,  croupous 
pneumonia  and  certain  other  infectious  inflammations.  The 
lesions  of  the  cornea  may  be  due  to  an  extension  of  the  inflamma- 
tion to  this  from  the  iris  and  ciliary  region,  which  was 
undoubtedly  true  in  one  case  examined.  The  third  cause  of  the 
eye  lesions,  and  that  to  which  most  of  the  cases  of  keratitis  in 
meningitis  are  due,  is  neuritis  of  the  fifth  nerve,  with  destruction 
of  the  Gasserian  ganglion  and  loss  of  sensation.  There  are  no 
lesions"  due  to  tropho-neurosis.  Purulent  conjunctivitis,  which  is 
frequently  found,  may  also  be  due  to  this  lack  of  sensation.  We 
have  but  one  record  of  the  examination  of  the  pus  from  the  con- 
junctiva, and  in  this  case  no  diplococci  were  found  in  the  pus. 


148 


EAR   COMPLICATIONS   IN  MENINGITIS. 

The  symptoms  relating  to  the  ears  play  an  important  part  in 
all  the  descriptions  of  meningitis.  That  there  should  be  dis- 
orders of  hearing  is  apparent  from  the  study  of  the  lesions. 
In  all  the  post-mortem  examinations  made  by  us  in  which  the 
auditory  nerves  were  examined  there  was  a  greater  or  less  degree 
of  involvement.  The  nerve  was  generally  swollen  and  surrounded 
by  exudation.  Microscopic  examination  showed  in  some  cases 
purulent  exudation  along  the  nerve  sheath,  with  more  or  less 
complete  destruction  and  infiltration  of  the  nerve.  The  studies 
of  nerve  degeneration  showed  extensive  degeneration  of  the 
nerve  fibres  in  all  cases  examined,  the  degeneration  being  most 
marked  in  the  more  chronic  cases.  The  bony  ear  was  saved  for 
examination  in  a  number  of  cases,  but  it  has  not  been  possible 
to  complete  the  microscopic  examination.  This  has  been  done 
by  others,  however,  in  a  number  of  cases,  and  the  anatomical 
foundation  of  the  ear  symptoms  has  been  established. 

The  first  investigation  on  the  condition  of  the  internal  ear  in 
epidemic  cerebro-spinal  meningitis  comes  from  Heller,^"-  who 
examined  the  ears  in  two  cases  in  the  epidemic  in  Erlangen  in 
1865.  In  both  he  found  acute  purulent  inflammation  of  the 
labyrinth,  which  he  thought  was  due  to  the  extension  of  the 
inflammation  from  the  brain  along  the  nerve.  Schwabach^**^ 
gives  a  more  detailed  account  of  the  examination  of  the  ears 
in  a  case  of  otitis,  which  developed  in  the  course  of  an  attack 
of  meningitis.  The  symptoms  of  ear  trouble  developed  seven 
days  after  the  beginning  of  the  attack,  and  consisted  in  throbbing, 
drumming,  difficulty  of  hearing  and  unbearable  pain.  Death 
took  plac3  five  weeks  after  the  beginning  of  the  disease.  He 
found  great  hypersemia  of  the  vessels  in  the  course  of  the 
acoustic  nerves  and  in  all  parts  of  the  labyrinth,  purulent 
inflammation  of  the  sheath  of  the  acoustic  and  ecchymoses 
between  the  fibres.  There  was  abundant  formation  of  granula- 
tion tissue  in  some  of  the  branches  of  the  nerves  and  in  the 
ganglia,  combined  with  suppuration  and  haemorrhage.  Pus  was 
found  in  the  peri-lymphatic  spaces  of  the  scala  and  other  parts. 


149 

There  was  slight  purulent  infiltration  of  the  sheath  of  the 
facial  nerve  on  the  right  side.  In  the  pus  taken  from  the 
middle  ear  by  puncture  of  the  drum  he  found  enclosed  in  the 
cells  diplococci  which  he  says  resembled  the  pneumococci.  (It  is 
most  probable  that  this  was  the  diplococcus  intracellularis.) 
Lucae^'^  examined  the  ears  in  a  case  of  cerebro-spinal  menin- 
gitis which  was  fatal  in  twenty-four  hours.  At  the  post-mortem 
examination  he  found  a  purulent  infiltration  of  the  meninges 
which  extended  along  the  facial  and  acoustic  nerves.  The  exu- 
dation extended  along  the  acoustic  to  the  cochlea  and  vestibule, 
and  into  the  semi-circular  cauaL  There  was  no  alteration  of 
the  middle  ear  or  of  the  drum  membrane. 

An  interesting  case  is  that  reported  by  Schultze,™  who  ex- 
amined the  ears  of  a  deaf-mute,  five  years  after  an  attack  of 
meningitis,  to  which  the  condition  was  due.  There  was  atrophy 
of  both  auditory  nerves  and  formation  of  granulation  tissue  in 
the  labyrinth.  Nothing  remained  of  the  organ  of  Corti.  The 
cavity  of  the  cochlea  was  filled  with  osteoid  tissue  and  round 
cells. 

Kochner  says  in  the  disease  of  the  ear  which  follows  menin- 
gitis there  may  be  ecchymoses  with  thickening  and  softening  of 
the  membranous  part  of  the  labyrinth.  Moos''^  says  the  inflam- 
mation extends  along  the  perivascular  and  perineural  lymphatics 
from  the  brain  to  the  ear.  From  the  perineurium  of  the  acoustic 
nerve  the  disease  extends  to  the  labyrinth.  Merkel  has  found 
destruction  of  the  semi-circular  canals  in  one  ear. 

In  all  these  investigations  it  has  generally  been  seen  that  the 
disease  of  the  ear  was  secondary  to  the  meningitis,  and  due  to 
extension  of  the  inflammation  from  the  brain  to  the  ear  along 
the  nerves  ;  or,  as  Mosler''-^  has  suggested,  to  an  involvement  of 
the  strise  acoustics  in  the  fourth  ventricle.  There  was  nothing 
found  in  our  cases  which  spoke  in  favor  of  this  view  of  Mosler. 

Some  confusion  has  existed  in  the  minds  of  writers  as  to  the 
relation  between  otitis  and  meningitis,  some  regarding  the  ear 
affections  as  primary,  others  as  secondary  to  the  meningitis. 
There  are  forms  of  meningitis  which  are  secondary  to  ear  dis- 
ease, and  result  from  the  extension  of  the  inflammation  in  the 


150 

ear  to  the  brain.  The  infection  in  these  cases,  according  to 
Korner,^'^  may  take  place  by  contact  with  the  diseased  bone 
or  by  extension  of  the  suppuration.  In  all  the  cases  which 
we  have  seen  of  this,  the  infectious  organism  was  either  the 
pneumococcus  or  the  streptococcus.  The  ear  lesions  of  epidemic 
cerebro-spinal  meningitis  are  always  secondary. 

Voltoline^'^^  described  as  an  independent  disease  inflammation 
of  the  labyrinth,  beginning  with  intense  pain  in  the  head, 
vomiting,  high  fever  and  convulsions.  It  lasts  for  some  days, 
and  usually  ends  in  recovery.  It  often  leaves  deafness  and 
uncertain,  trembling  gait.  One  of  the  chief  points  which  makes 
Voltoline  regard  this  as  an  independent  disease,  and  not  as  a 
complication  of  meningitis,  is  that  it  only  affects  children,  and 
in  a  short  time  tends  to  recovery.  He  finds  that  herpes  of  the 
lips,  so  common  in  meningitis,  is  rare  in  the  labyrinth  disease. 
In  the  ear  disease  vomiting  is  constant  and  may  be  absent  in 
meningitis.  This  view  has  been  shown  to  be  erroneous  by  Moos 
and  by  Leichtenstern.  Leichtenstern  says  there  are  slight  abortive 
cases  of  epidemic  cerebro-spinal  meningitis  which  lead  to  deafness 
in  consequence  of  a  simultaneous  affection  of  the  labyrinth,  so 
that  the  affection  of  the  labyrinth  may  seem  to  be  the  most 
important  or  primary. 

These  ear  lesions  are  the  most  common  of  the  complications 
of  meningitis.  Schwabach^**^  found  that  one-half  the  cases  of 
deaf -mutism  were  the  result  of  disease  of  the  central  nervous 
system.  Moos'"'  found  that  of  sixty-four  cases  of  meningitis 
which  recovered  fifty-nine  per  cent,  were  deaf,  thirty-one  per 
cent,  had  normal  hearing  and  in  seven  the  hearing  was  im- 
paired. Out  of  forty-three  cases  deafness  appeared  in  two  on 
the  first  day,  in  six  on  the  second,  in  three  on  the  third,  in 
seventeen  between  the  fourth  and  tenth  and  in  fifteen  between 
the  fourteenth  day  and  the  fourth  month.  He  thinks  that  it  is 
possible  that  the  abortive  form  of  epidemic  cerebro-spinal  men- 
ingitis is  the  cause  of  many  cases  of  early  acquired  deafness. 
Erhardt  observed  twenty-seven  cases  of  deafness  after  cerebro- 
spinal meningitis,  and  comes  to  the  conclusion  that  the  severity 
of  the  disease  stands  in  no  relation  to  the  deafness.     The  deaf- 


151 

ness  appears  suddenly,  without  pain,  and,  as  a  rule,  in  the  be- 
ginning of  the  disease.  Jackson^'  found  purulent  discharge 
from  the  ears  in  a  number  of  cases,  and  in  a  few  there  was 
deafness  on  recovery.  Friis^  found  seven  cases  of  ear  disease 
in  thirty  cases  investigated  by  him.  Of  those  that  recovered, 
two  had  otitis  media,  one  otitis  interna  and  one  was  partially 
deaf  without  discoverable  cause.  Kuapp^*^  reports  a  case  of 
unilateral  deafness.  The  character  of  the  disorders  of  hearing 
has  been  investigated.  Kochner  found,  in  the  cases  studied  by 
him  in  Wurzburg,  many  variations  in  the  character  of  sound 
perception.  There  were  transitions  from  more  or  less  difficult 
hearing  to  absolute  deafness.  When  deaf  to  ordinary  sounds, 
patients  could  often  distinctly  hear  scratching  noises.  Bliimm^ 
describes  buzzing  and  hammering  in  the  ears  and  hallucinations 
of  hearing.  Mosler'^  gives  the  history  of  a  case  with  slow  re- 
covery. At  first  there  was  total  deafness,  after  a  time  loud 
sounds  could  be  distinguished ;  there  was  ringing  in  the  ears 
during  the  entire  time.  The  walk  was  at  first  trembling  and 
uncertaio,  but  gradually  became  better.  Gahlberg^  reports  the 
case  of  a  child  three  years  old  which  recovered,  having  a  totter- 
ing, swaying  motion  and  a  tendency  to  turn  in  a  circle.  The 
disease  of  the  internal  ear  may  or  may  not  extend  to  the 
middle  ear. 

In  the  notes  on  our  cases  pathological  conditions  relating  to  the 
ears  are  mentioned  sixteen  times.  The  conditions  found  varied 
from  pain  and  mastoid  tenderness  to  deafness  with  or  without 
otitis  media.  One  case  was  operated  on  for  mastoiditis,  and  pus 
was  found  in  the  sinuses.  Otitis  media  developed  in  five  cases, 
and  in  three  of  these  the  pus  was  examined  for  diplococci.  The 
organisms  were  found  enclosed  in  pus  cells  in  all  three  of  the 
cases  examined.  These  cases  of  secondary  otitis  media  with 
diplococci  in  the  pus  cells  are  important,  from  the  possibility  of 
further  infection  which  they  offer.  They  also  furnish  proof  of  the 
extension  of  the  infection  from  the  brain. 


152 


NOSE  AND  THROAT. 

Acute  Coryza. 

There  is  but  little  mention  of  acute  coryza  as  a  complication. 
Richter  reports  that  in  all  his  cases  there  was  coryza  in  the 
beginning,  and  nasal  catarrh  was  sometimes  seen  among  the 
prodromata.  Strlimpel  says  that  in  a  number  of  his  cases  menin- 
gitis was  preceded  by  nasal  catarrh,  and  in  one  case  there  was 
marked  disturbance  of  smell.  This  matter  is  of  interest,  in  view 
of  the  opinion  which  was  first  advanced  by  Weigert,  that  in 
meningitis  the  nose  forms  the  portal  of  entry  for  the  infectious 
organisms.  In  our  cases  acute  coryza  is  mentioned  but  once. 
There  were  three  cases  of  epistaxis,  and  in  one  this  was  among  the 
first  symptoms  noted. 

Scherrer  examined  the  noses  in  eighteen  cases,  and  in  the 
secretion  of  all  found  pus  cells  with  diplococci.  He  believes  that 
this  examination  of  the  nose  is  one  of  the  most  important  points 
in  the  diagnosis  of  the  disease. 

The  nasal  secretion  of  nineteen  of  our  cases  was  examined  by 
means  of  cover-glass  preparations.  The  preparations  were  stained 
first  by  Gram's  method  and  afterwards  with  a  solution  of  Bismarck 
brown,  as  in  the  method  for  the  examination  of  urethral  pus  for 
gonococci. 

The  material  for  examination  was  obtained  in  most  instances 
from  the  higher  portions  of  the  nasal  cavities,  with  the  aid  of  the 
platinum  "loop." 

Of  the 'fifteen  cases,  ten  showed  the  presence  in  the  nasal 
secretion  of  diplococci,  decolorizing  by  Gram's  method,  and  iden- 
tical in  morphology  with  the  diplococcus  intracellularis  menin- 
gitidis. They  occurred  as  a  rule  in  small  numbers,  and  were  very 
frequently  observed  inside  of  polynuclear  leucocytes. 

Similar  Gram  decolorizing  diplococci  were  also  found  within 
leucocytes  in  the  nasal  secretions  of  two  cases  of  convalescent 
meningitis.  Attempts  were  made  to  isolate  this  diplococcus  by 
cultures  in  ten  cases  in  which  the  microscopical  examination 
showed  it  to  be  present,  but  without  success.     This  was  probably 


153 

due  to  the  large  number  of  colonies  of  other  bacteria  which 
developed  and  to  the  relatively  small  number  of  the  diplococci. 

With  reference  to  the  occurrence  of  this  organism  in  the  nasal 
secretions  of  patients  not  affected  with  meningitis,  twelve  hospital 
patients,  chosen  at  random,  were  examined.  In  the  nasal 
secretions  of  two  among  these  twelve  diplococci-  like  the 
preceding  were  found  by  cover-glass  examination.  They  were 
not   cultivated. 

From  the  results  of  these  examinations  it  would  seem  either 
that  the  diplococcus  intracellularis  may  be  met  with  in  the  nasal 
secretion  of  patients  who  have  not  meningitis,  or  that  other 
species  of  diplococci  identical  with  this  morphologically  and  in 
staining  peculiarities  may  be  found  there.  It  is  greatly  to  be 
regretted  that  it  was  not  possible  to  obtain  cultures  of  the 
organisms  from  this  locality,  for  only  by  that  method  combined 
with  inoculations  can  the  identity  be  established.  At  any  rate,  it 
is  impossible  to  regard  the  presence  of  diplococci  decolorized  by 
the  Gram  stain  in  the  nose  as  of  much  diagnostic  value,  as  has 
been  claimed  by  Scherrer. 

The  mucous  membrane  was  examined  microscopically  four 
times,  and  in  one  case  pus  cells  and  small  numbers  of  diplococci 
were  found.  In  three  other  cases  in  which  the  membrane  was 
examined  at  autopsy  no  inflammatory  condition  was  found.  The 
relation  of  acute  coryza  to  meningitis  is  of  great  importance,  and 
it  is  one  point  which  must  be  cleared  up  in  the  future  investigation 
of  the  disease.  Even  assuming  that  the  organisms  found  in  the 
nose  were  certainly  the  diplococcus  intracellularis  meningitidis  it 
would  seem  that  the  presence  of  an  acute  Coryza  with  organisms 
in  the  pus  cells  is  not  a  conclusive  proof  that  the  nose  forms  the 
portal  of  entry  for  the  organisms.  The  acute  coryza  can  be  just 
as  well  a  secondary  complication,  and  due  to  the  entry  of  the 
organism  into  the  nose  from  the  brain. 

Inflammation  of  the  throat  is  frequently  mentioned  in  the  earlier 
accounts  of  the  epidemics,  but  not  in  the  latter.  Jackson  says 
that  patients  often  complain  of  sore  throat,  and  the  fauces  were 
often  found  red  and  inflamed.  North  says  that  aphthous  patches 
were  often  seen  in  the  throat.     In  one  of  Daga's  cases  there  were 


154 

small  abcesses  in  the  tonsils.  Lavaran  says  that  the  tonsils  are 
frequently  the  seat  of  small  abcesses.  Faure-Villar  ^^  mentions  a 
case  in  which  there  was  gangrenous  pharyngitis  complicating  the 
disease.  In  one  case  reported  by  Senator  ^"^  there  were  drops  of 
pus  in  the  tonsils.  Swelling  and  abscess  of  the  tonsil  were  found 
in  one  of  our  cases  at  autopsy,  and  a  culture  from  the  abscess 
material  showed  the  presence  of  diplococci.  The  tissue  was  not 
examined  microscopically. 

JOINTS. 

Acute  inflammation  of  the  joints  is  frequent  in  meningitis. 
Jackson  says  in  some  cases  the  joints  and  limbs  were  swollen,  and 
resembled  gout.  North  describes  swelling  of  the  joints,  resem- 
bling acute  rheumatism.  Lavaran  says  that  acute  articular  rheum- 
atism was  very  common  at  the  same  time  with  the  epidemic  of 
meningitis,  and  was  found  as  a  complication  in  one  of  the  cases  of 
meningitis.  In  three  of  the  cases  reported  by  Richter^^  there  was 
acute  inflammation  of  the  joints.  In  one  it  appeared  on  the  sixth 
day.  Kotsonopulos,^"^  in  the  epidemic  observed  by  him  at  Naup- 
lia,  Greece,  found  acute  inflammation  of  the  joints  in  a  large 
proportion  of  his  cases.  He  gives  no  anatomical  description  of  the 
lesions.  Striimpel  found  multiple  swelling  of  the  joints  in  several 
cases.  In  one  of  the  cases  reported  by  Friis  there  was  an  inflam- 
matory exudation  in  the  knee  joint,  but  no  organisms  were  found 
in  the  synovia  examined.  Berg  says  that  in  the  epidemic  in  New 
York,  in  1895,  affections  of  the  joints  were  present  in  most  of  the 
cases  which  he  saw.  The  knees  were  most  commonly  affected ; 
and  the  condition  varied  from  pain  to  swelling,  redness,  and  con- 
ditions simulating  acute  articular  rheumatism.  Levy  found  pus  in 
the  joints  twice.  In  one  case  there  was  phlegmonous  pus  in  almost 
all  the  joints,  extending  into  the  sheaths  of  the  tendons.  There 
are  no  records  of  any  microscopic  examination  of  these  joints,  and 
the  only  record  of  an  examination  of  the  pus  for  organisms  is  that 
given  by  Friis.  In  six  of  our  cases  acute  inflammation  of  the  joints 
was  found.  Five  of  these  cases  recovered.  At  all  of  the  post- 
mortem examinations  the  articulations  were  examined  with  great 


155 

care,  bnt  no  lesions  were  fouud  in  them.  It  is  greatly  to  be  re- 
gretted that  the  opportunity  was  not  given  for  careful  bacterio- 
logical and  histological  examination  of  this  interesting  condition, 
to  ascertain  its  cause  and  its  relation  with  the  other  lesions  of  the 
disease. 

BLOOD. 

Blood  counts  were  made  in  thirty-three  cases.  In  many 
of  these  a  number  of  counts  were  made  at  varying  intervals 
throughout  the  disease.  Leucocytosis  was  always  present.  The 
highest  number  of  leucocytes  in  any  case  was  31,000  ;  the  smallest 
number  was  9,350.  In  general,  when  several  blood  counts  were 
made  during  the  course  of  the  disease  it  was  found  that  the 
leucocytes  gradually  diminished  towards  the  end  of  the  disease 
in  those  cases  which  recovered.  Differential  counts  showed  that 
the  increase  was  due  to  the  polynuclear  leucocytes. 

PULSE   AND   TEMPERATURE. 

There  was  no  careful  study  of  the  temperature  of  the  disease 
until  the  epidemic  in  Leipzig  in  1863  and  1864,  in  which  the  pulse 
and  temperature  were  carefully  studied  by  Wunderlich.  Jackson 
says  that  there  seemed  to  be  a  great  deal  of  variation  in  the  bodily 
temperature.  North  says  but  little  on  the  presence  and  character 
of  the  fever.  Wunderlich^*  found  in  his  studies  of  the  tempera- 
ture that  the  fever  has  nothing  characteristic,  and  shows  a  marked 
degree  of  difference,  according  to  the  development  and  the  dura- 
tion of  the  disease.  He  thinks  that  marked  differences  in  the 
course  of  the  fever  may  be  due  to  complications  of  the  disease. 
Exacerbations  of  the  nervous  symptoms  are  not  always  coincident 
with  a  rise  of  temperature.  The  fever  can  have  the  course  and 
the  exacerbations  and  may  attain  the  height  of  a  typhoid  tempera- 
ture, but  the  curve  varies  materially  from  this.  It  is  more  similar 
to  the  fever  in  tuberculosis,  and  in  no  place  shows  the  regularity, 
of  the  typhoid  curve.  The  most  marked  characteristic  of  the  dis- 
ease is  the  inequality  between  the  pulse  and  temperature.  The 
fever  is  of  short  duration,  and,  while  the  temperature  may  reach 


156 

a  considerable  height,  the  pulse  often  remains  normal.  In  the 
article  by  Striimpel  there  is  also  an  interesting  study  of  tempera- 
tures. He  finds  no  relation  between  the  height  of  the  fever  and 
the  severity  of  the  other  symptoms.  He  gives  a  temperature 
chart,  in  what  he  speaks  of  as  the  abortive  type,  in  which  there  is 
a  temperature  up  to  1054°  on  the  third  day,  and  on  the  sixth, 
normal  temperature. 


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He  says,  on  the  one  hand,  that  severe  cases  may  have  a 
rapid  course  with  but  little  fever ;  and,  on  the  other  hand,  very 
mild  cases  may  have  high  fever.  In  a  number  of  cases  there 
was  no  relation  between  the  degree  of  fever  and  the  other 
symptoms.  The  accompanying  curve,  which  is  taken  from 
Striimpel,  gives  an  example  of  a  very  severe  case,  ending  fatally 
with  but  slight  fever.  It  is  possible  for  the  most  severe  cases 
to  run  their  course  without  any  or  very  slight  increase  of   tem- 


157 


perature.  The  fever  may  suddenly  drop,  but  the  symptoms  do 
not  abate  ;  for  weeks  there  may  be  severe  disturbances  of  con- 
sciousness, delirium,  opisthotonos  and  headache,  while  the  fever 
has  long  ceased  or  the  temperature  has  even  become  sub-normal. 
In  one  of  his  cases  which  ended  fatally,  there  was  a  sub- 
normal temperature  throughout.  The  autopsy  in  this  case  showed 
a  very  marked  purulent  infiltration  of  the  meninges  everywhere, 
and  he  thinks  that  the  absence  of  fever  may  be  explained  by  a 
direct  influence  of  the  lesions  on  the  heat-regulating  centre.  A 
large   number  of   severe    and  medium   cases   shows   the  type   of 


CHART  H 


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remittent  fever.  The  temperature  rarely  reaches  the  height  of 
104°  and  varies  between  102.2°  and  100.4°.  Sometimes  this 
course  is  interrupted  by  deep  remissions.  In  these  cases  the 
curve  has  a  certain  similarity  with  the  curve  in  mild  cases  of 
typhoid.  The  fever  ceases  gradually,  and  the  fall  is  interrupted 
by  irregular  rises  and  falls.  Striimpel  has  seen  cases  of  typical 
intermittent  character,  and  the  intermissions  took  place  in  the 
morning  and  forenoon.  He  gives  two  cases  showing  typical 
intermissions.  Both  recovered.  A  terminal  rise  of  temperature 
was  seen  in  a  number  of  his  cases,  and  he  gives  the  curve  of 
one  case  in  which  there  was  a  rise  to    107f°.     (Chart  III.) 


158 


Grimsbaw,"^  in  his   study   of   the   temperature   in  the  disease, 
concludes  that  there    is  no   typical   temperature  chart.     In  mild 

cases  the  fever  seldom  exceeds 


c. 


CHA-RT  n- 

4  5 


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100°.  In  some  rapidly  fatal 
cases  103°  was  found,  and  in 
none  was  there  a  temperature 
of  over  104°.  The  degree  of  the 
0  temperature  and  the  rapidity  of 
the  pulse  have  not  that  accord 
usually  found  in  acute  diseases. 
Variations  in  temperature  sel- 
dom precede  but  usually  ac- 
company variations  in  other 
symptoms.  Low  temperatures 
»rtn  n"  frequently  indicate  severe  cases, 
as  do  temperatures  over  104°, 
and  frequent  variations  of  tem- 
operature  indicate  a  severe  and 
prolonged  case  with  doubtful 
result. 
„  Hermann  and  Kober^  say  that 
98' 6  the  temperature  is  never  typical. 
Some  cases  begin  with  chill  and 
high  temperature,  others  with 
sub-normal  temperature.  The  curve  of  the  temperature  in  the 
course  of  the  disease  is  always  irregular.  There  are  remissions 
and  exacerbations,  sometimes  continuous  sub-normal  tempera- 
tures, and  at  others  the  curve  shows  the  type  of  continued  fever, 
with  a  temperature  of  102.2°  to  104°.  Levy®  says  the  disease 
frequently  begins  with  chill ;  the  temperature  in  general  is  not 
high  and  the  pulse   is  slow. 

Gahlberg,  in  the  epidemic  of  Mailburg,  found  the  temperature 
low,  usually  not  exceeding  102.2°.  Hermann^^  reports  one  case 
in  which  the  temperature  was  very  high,  reaching  113°.  In  the 
cases  reported  by  Berg^  in  New  York,  in  1893,  he  found  in  some 
rapid  rise  and  fall  of  temperature.  As  a  rule  the  temperature 
was   not   high,  but   cases  dying   in   a   comatose    condition   as  a 


41 


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159 

rule  have  high  temperatures,  up  to  106°  or  over.  Most  of 
Berg's  observations  were  made   on  children. 

Bungeroth  says  many  cases  begin  with  chill  and  sudden  increase 
of  temperature,  while  in  others  the  temperature  is  scarcely  raised 
above  normal,  and  it  gradually  increases,  sometimes  to  a  consider- 
able degree.  In  the  first  report  by  Leichtenstern  of  the  cases  in 
Cologne  he  says  that  the  fever  is  exceedingly  irregular  and  atypical, 
and  not  always  proportionate  to  the  severity  of  the  case.  Severe 
and  fatal  cases  may  show  for  some  time  a  sub-normal  temperature, 
which  increases  rapidly  at  the  end.  In  some  of  his  cases  there  was 
agonal  and  post-mortem  elevations  of  temperature.  Sub-febrile 
temperatures  were  often  interrupted  by  a  rapid  rise,  which  could 
take  place  at  any  time  of  the  day  or  night.  Sometimes  there  were 
marked  daily  variations  at  irregular  intervals. 

The  pulse  shows  the  same  irregularity  as  the  temperature,  and 
in  all  the  epidemics  observers  have  agreed  that  there  is  no  relation 
between  the  pulse  and  temperature,  such  as  is  seen  in  acute  febrile 
diseases.  North  says  the  pulse  is  often  soft  and  weak,  slow  or 
slower  than  in  health,  often  intermittent  and  fluttering.  Jackson 
says  there  is  great  irregularity  in  the  pulse,  and  its  character  and 
rapidity  vary  at  short  intervals.  Wunderlich  says  that,  while  the 
temperature  may  reach  a  considerable  height,  the  pulse  often  re- 
mains normal  or  even  under  normal,  and  this  relation  is  not  met 
with  in  any  other  disease.  Bungeroth  says  it  was  constantly 
observed  that  the  pulse  was  soft  and  small  in  the  beginning  of  the 
disease.  In  severe  cases  it  was  thread-like  and  could  scarcely  be 
felt.  In  fatal  cases  the  pulse  generally  becomes  rapid  and  inter- 
mittent, or  it  changes  suddenly  from  very  slow  to  very  rapid,  so 
that  in  a  minute  it  varied  from  70  to  130. 

Mankopf  observed  in  a  series  of  cases  that  the  rate  of  the 
pulse  in  the  beginning  of  the  disease  was  diminished,  so  that  even 
in  high  temperatures  at  the  beginning  of  the  disease  the  pulse 
scarcely  reached  normal,  and  might  be  below  it.  In  almost  all 
of  the  fatal  cases  the  rate  of  the  pulse  went  up  to  over  120, 
while  at  the  same  time  the  temperature  fell.  Leichtenstern  found 
that  the  pulse  varied  enormously.  Changes  from  80  to  100  in  the 
following  minute  were  seen.     Absolute  slowness  of  the  pulse  was 


160 

not  common.  Eelative  slowness  in  relation  to  the  temperature 
was  found  often,  especially  in  children.  In  two  cases  reported  by 
Presse  ^^  there  was  strong  pulsating  movement  of  the  entire  head, 
and  in  a  child  seen  by  Danielson  and  Mann  there  was  such  strong 
pulsation  that  the  fontanells  bulged. 

The  slight  variations  in  these  descriptions  of  the  pulse  and 
temperature  are  probably  due  to  the  small  number  of  cases 
seen  by  some  observers.  In  going  over  the  histories  of  the 
cases  we  have  carefully  studied  the  attached  charts,  and  the 
extraordinary  irregularity  of  the  temperature  is  most  striking. 
Single  charts  might  be  selected  which  for  a  week  or  more  show 
a  curve  very  similar  to  that  of  typical  cases  of  typhoid  fever. 
We  have  appended  a  number  of  charts  of  pulse  and  tempera- 
ture to  the  description  of  the  individual  cases,  which  will  give 
a  fair  idea  of  the  great  variability  of  both  pulse  and  tempera- 
ture. These  record  the  morning  and  evening  temperatures, 
and  the  four-hour  charts  show  the  same  irregularity.  In  one 
case  there  was  a  rise  of  5°  during  the  visit  of  the  attending 
physician.  None  of  these  curves  shows  the  temperature  for  the 
whole  period  of  the  disease.  A  variable  length  of  time,  from 
one  day  to  several  weeks,  elapsed  from  the  onset  of  the  dis- 
ease until  the  patient  entered  the  hospital.  It  would  be  very 
important  to  have  a  few  observations  of  temperature  from  the 
onset.  All  the  observations  on  temperature  which  have  been 
recorded  were  made  on  hospital  patients  in  all  of  whom  the 
beginning  of  the  fever  would  be  lost.  These  variations  in  tem- 
perature do  not  seem  to  have  been  dependent  upon  complications 
of  the  disease.  In  one  case  the  onset  of  acute  croupous  pneu- 
monia was  marked  by  a  sudden  rise  in  the  temperature.  While 
we  believe  that  it  would  not  be  possible  from  a  single  temperature 
to  diagnose  the  character  of  the  disease,  the  observation  of  a  num- 
ber of  charts  in  an  epidemic  would  enable  us  to  be  certain  of  its 
character. 

MENTAL    CONDITION    ON    RECOVERY. 

The  influence  of  epidemic  meningitis  in  producing  a  permanent 
impairment  of  the  mind  has  not  received  the  attention  it  should 


161 

have.  It  is  certain  that  pathological  alterations  may  be  pro- 
duced in  the  brain  which  are  not  easily  recovered  from.  Baxa 
found  that  the  disease  was  sometimes  followed  by  idiocy.  Ac- 
cording to  Bliimm,  the  influence  of  the  disease  on  the  intelligence 
may  be  marked.  In  our  cases  there  are  four  notes  on  abnormal 
mental  conditions  of  patients  at  the  time  of  discharge  from  the 
hospital.  Marked  mental  impairment  was  noted  in  two  cases, 
a  third  was  irrational  and  childish  and  a  fourth  was  stupid  and 
did  not  recognize  his  relatives.  None  of  these  cases  could  be  fol- 
lowed up,  to  see  whether  the  mental  disturbance  was  permanent. 

DIAGNOSIS. 

The  diagnosis  of  typical  cases  of  epidemic  meningitis  is  easy, 
and  other  diseases  should  not  be  confounded  with  it.  Krannhals^^ 
says  there  may  be  symptoms  exactly  resembling  those  of  menin- 
gitis, without  the  anatomical  lesions.  He  gives  the  clinical 
history  of  seven  such  cases,  with  six  deaths.  It  is  diflBcult  to  say 
on  what  grounds  the  diagnosis  of  meningitis  was  made  in  the 
cases  which  died.  Suddenness  of  attack,  vomiting,  pain  and 
stiffness  of  neck,  inequality  of  the  pupils,  irregularity  of  the 
pulse  and  temperature  were  all  lacking.  There  was  headache, 
partial  coma,  delirium,  clonic  convulsions,  clonic  stiffness  of  the 
muscles.  In  every  case  the  spleen  was  enlarged,  and  in  one  case 
very  much  so.  In  the  case  which  recovered  the  symptoms  very 
much  resembled  those  of  cerebro-spinal  meningitis.  He  says  that 
during  the  epidemic  of  influenza  in  Riga,  in  1889  and  1890,  there 
were  six  cases  diagnosed  as  meningitis.  One  of  these  cases 
proved  to  be  endocarditis,  one  pneumonia  and  the  four  others  true 
cases  of  meningitis. 

Koht"^  speaks  of  a  case  of  influenza  in  which  there  were  typical 
symptoms  of  meningitis,  but  the  autopsy  showed  only  hypersemia. 

Striimpel  says  there  may  be  a  clinical  picture  of  a  primary 
acute  cerebral  disease  without  appreciable  cause,  so  that  a 
diagnosis  of  acute  meningitis  is  apparently  justified,  and  the 
autopsy  may  be  entirely  negative  with  the  exception  of  hypersemia 
or  oedema  or  some  such  slight  alteration. 


162 

Hermann  thinks  that  the  diagnosis  is  easy  in  general,  but  in 
children  may  be  confounded  with  tubercular  meningitis  ;  and  some 
of  the  cases  with  abundant  skin  eruption  may  be  confounded  with 
typhoid. 

It  is  difficult  to  make  an  absolute  diagnosis  of  any  disease  from 
the  symptoms  alone.  The  surest  method  of  diagnosis,  and  one 
which  should  always  be  carried  out  when  possible,  is  by  lumbar 
puncture.  The  method  is  easy,  and  experience  has  shown  it  to  be 
devoid  of  danger.  If  properly  carried  out  in  the  early  stages  of 
the  disease,  which  is  the  time  when  there  is  most  difficulty  in 
diagnosis,  it  is  almost  conclusive.  It  certainly  deserves  to  be 
ranked  as  a  method  of  diagnosis  with  the  examination  of  the 
sputum.  If  the  patient  has  meningitis,  a  more  or  less  cloudy  fluid 
will  be  withdrawn.  If  it  is  the  epidemic  form,  diplococci  will  be 
found  in  it  either  on  microscopic  examination  or  in  cultures.  It 
is  of  the  greatest  importance,  in  the  study  of  the  epidemics  that 
this  method  of  diagnosis  should  be  carried  out  especially  in  the 
sporadic  cases.  In  some  of  the  chronic  cases  if  seen  late  there 
may  be  a  question  of  diagnosis  between  meningitis  and  typhoid 
fever. 

SUMMARY. 

Epidemic  cerebro-spinal  meningitis  is  an  acute  infectious  disease, 
which  is  produced  by  a  micrococcus  characterized  by  its  growth  in 
pairs  and  by  certain  cultural  and  staining  properties.  The  organ- 
ism, so  far  as  we  can  tell  by  laboratory  experiments,  is  one  of 
feeble  vitality,  but  it  must  be  remembered  that  we  cannot  produce 
in  the  laboratory  exactly  the  same  conditions  that  the  organism 
might  find  in  nature.  The  essential  seat  of  the  disease  is  in  the 
meninges  of  the  brain  and  cord.  How  the  organism  gains  access 
to  the  meninges  is  not  actually  known.  It  is  possible  that  the 
nose  forms  the  portal  of  entry,  the  organism  passing  from  the  nose 
to  the  meninges  by  means  of  the  lymphatics  connecting  this  with 
the  subdural  spaces.  In  a  number  of  cases  organisms  identical 
with  it  on  microscopical  examination,  have  been  found  in  the  nose 
together  with  evidences  of  slight  acute  inflammation.      These  or- 


163 

ganisms  have  not  been  cultivated  and  have  been  found  in  other 
diseases.  The  lesions  in  the  meninges  are  confined  to  the  pia- 
arachnoid,  in  which  an  acute  purulent  inflammation  is  produced. 
From  the  meninges  the  process  extends  into  the  brain  substance. 
Lesions  are  found  not  only  in  the  cortex  but  in  the  depth  of  the 
tissue  and  in  the  ventricles.  These  lesions  consist  in  part  of  pur- 
ulent infiltration  of  the  tissue  both  around  the  vessels  and  else- 
where, together  with  proliferative  changes  in  the  neuroglia  and 
degenerative  changes  in  the  ganglion  cells  and  nerve  fibres.  The 
cord  is  always  affected,  and  to  a  greater  extent  than  in  any  of  the 
other  forms  of  meningitis.  The  organisms  are  found  in  consider- 
able numbers  in  the  most  acute  cases.  In  the  more  chronic  cases 
they  may  be  missed.  Probably  the  surest  method  of  diagnosis  in 
the  disease  is  that  by  spinal  puncture.  If  the  puncture  be  made  in 
an  early  stage  of  the  disease,  a  fluid  more  or  less  clouded  by  the 
presence  of  pus  cells  will  be  found,  and  in  these  pus  cells  there  are 
variable  numbers  of  the  organisms.  In  many  cases  the  growth  of 
the  organism  is  so  feeble  that  great  care  must  be  exercised  in  mak- 
ing the  cultures,  and  large  amounts  of  the  fluid  used.  If  the  spinal 
puncture  be  made  late  in  the  disease,  the  results  may  be  negative. 
The  disease,  especially  in  its  chronic  form,  is  characterized  by 
remissions  and  exacerbations.  Spinal  puncture  may  be  negative 
if  made  during  a  remission,  and  positive  in  the  exacerbation. 

A  marked  feature  in  the  pathological  lesions  of  the  disease  is 
the  tendency  for  the  infection  to  extend  along  the  nerves,  particu- 
larly along  the  optic,  auditory  and  fifth  nerves.  By  its  extension 
along  the  optic  nerve  it  may  produce  a  purulent  inflammation  of 
the  orbit  or  a  purulent  inflammation  of  the  eye.  In  its  extension 
along  the  fifth  nerve  it  produces  an  acute  inflammation  of  the 
Gasserian  ganglion,  with  destruction  and  degeneration  of  the  nerve 
cells  composing  it.  By  its  extension  along  the  auditory  nerve  it 
may  lead  to  destruction  of  the  internal  auditory  apparatus,  with  or 
without  acute  inflammation  of  the  middle  ear.  In  the  acute  inflam- 
mation of  the  middle  ear,  which  appears  not  infrequently  as  a 
complication  of  the  disease,  diplococci  are  found  in  the  pus  cells. 
It  is  possible  that  the  presence  of  the  organisms  in  the  nose  is  to 
be  referred  to  such  an  extension,  and  not  to  a  primary  invasion. 


164 

The  organism  does  not  produce  a  general  septicaemia.  There  is 
no  general  invasion  of  the  other  tissues  of  the  body. 

The  organism  is  capable  of  entering  the  lung  and  producing 
a  focal  pneumonia  characterized  by  especial  anatomical  features. 
In  the  periphery  of  the  foci  there  is  a  hsemorrhagic  oedema  of 
the  tissue.  The  foci  vary  in  size  from  a  pea  or  a  bean  to  an 
involvement  of  the  lung  comparable  to  an  acute  croupous  pneu- 
monia. In  the  large  areas  of  consolidation  several  centres  are 
usually  found.  This  form  of  pneumonia  was  found  in  eight  of 
our  cases.  It  may  appear  either  in  the  very  acute  or  in  the  more 
chronic  cases.  It  seems  probable  from  the  microscopic  study 
of  the  lesions  that  the  organism  enters  the  lung  by  means  of 
the  blood  vessels  rather  than  by  the  bronchi.  The  possibilities  of 
bronchial  infection  are  given  by  the  presence  of  the  organism  in 
the  nose  from  which  it  could  easily  extend  into  the  bronchi,  and 
by  the  disease  of  the  middle  ear,  the  organisms  from  here  enter- 
ing the  throat  by  means  of  the  eustachian  tube. 

The  symptoms  of  the  disease  are  those  which  might  be  ex- 
pected from  the  anatomical  lesions.  There  are  no  prodromata, 
and  the  usual  history  is  that  of  sudden  onset,  with  vomiting  and 
pain  in  the  head.  In  most  cases  there  is  pain,  stiffness  and  muscu- 
lar contraction  of  the  neck,  which  may  extend  to  the  muscles  of 
the  back  and  the  lumbar  region.  There  is  usually  delirium,  and 
in  many  cases  unconsciousness  passing  into  complete  coma. 
There  are  numerous  complications  in  the  disease.  Those  of  the 
eye  and  ear  are  easily  understood.  The  joint  complications 
which  are  seen  with  greater  or  less  frequency  in  some  epidemics 
(and  they  have  been  very  frequent)  cannot  be  explained.  No 
opportunity  was  given  in  the  study  of  the  epidemic  for  the  micro- 
scopic and  bacteriological  examination  of  these  joints. 

Degenerative  lesions  of  the  nerves  have  been  found  to  a  greater 
or  less  extent  in  all  the  cases  in  which  these  were  looked  for. 

The  cases  reported  were  seen  in  the  Boston  City  Hospital,  the 
Children's  Hospital  and  the  Massachusetts  General  Hospital.  Few 
cases  seem  to  have  been  seen  in  private  practice.  The  disease 
was  most  prevalent  among  the  poor,  and  the  cases  were  very 
generally  distributed  over  the  city. 


165 

Reports  as  to  the  contagiousness  of  the  disease  vary,  but  the 
general  opinion  is  that  the  disease  is  not  propagated  by  contagion. 
In  this  epidemic  there  were  seen  several  instances  in  which  two 
cases  came  from  the  same  house  and  family.  There  were  one 
hundred  and  eleven  cases  seen  in  the  epidemic,  and  of  these 
seventy-six  died  and  thirty-five  recovered,  making  a  mortality 
of  sixty-eight  per  cent. 

There  is  some  ground  for  the  assumption  that  many  of  the 
cases  of  sporadic  meningitis  are  of  the  epidemic  form.  The 
disease  may  be  present  in  a  community  and  only  show  itself  in 
scattered  sporadic  cases.  Then  under  favorable  conditions,  the 
nature  of  which  we  do  not  understand,  the  number  of  cases  may 
increase  to  an  epidemic.  The  epidemics  of  the  disease  usually 
last  more  than  a  year  and  slowly  decrease,  but  the  disease  does 
not  disappear.  The  mortality  is  high  and  varies  much  in  different 
epidemics,  ranging  from  twenty  to  seventy-five  per  cent.  So 
far  as  we  have  been  able  to  learn  from  a  review  of  the  literature 
methods  of  treatment  have  but  little  influence  on  the  mortality. 
The  disease  is  most  apt  to  appear  in  the  young,  cases  being  rare 
in  persons  over  thirty-five  j^ears  of  age. 

Meningitis  Due  to  Various  Infectious  Organisms. 

With  a  view  of  ascertaining  the  frequency,  together  with  the 
clinical  and  anatomical  features  of  cerebro-spinal  meningitis  due 
to  other  organisms  than  the  diplococcus  intracellularis,  we  have 
collected  a  number  of  cases  from  the  reports  of  the  laboratory 
for  the  past  five  years.  Most  of  those  cases  come  from  the 
Boston  City  Hospital,  but  a  number  of  them  are  from  private 
autopsies,  and  the  bacteriological  and  histological  examinations 
in  these  cases  were  made  at  the  Sears  Pathological  Laboratory 
of   the  Harvard  Medical  School. 

In  the  literature  of  meningitis  there  are  a  number  of  cases 
reported  of  infection  with  various  organisms,  but  there  is  sel- 
dom a  complete  description  from  both  a  clinical  and  anatomical 
point  of  view.  When  the  clinical  history  is  good,  the  bacterio- 
logical and  anatomical  investigation  has  usually  been  imperfectly 
carried   out,  and  vice  versa.     We  have   found   the   infection   of 


166 

the  meninges  to  be  most  commonly  caused  by  the  tubercle 
bacillus,  the  pneumococcus  and  the  streptococcus.  In  one  case, 
the  entire  history  of  which  is  very  imperfect,  there  was  a  mixed 
infection  with  the  bacillus  pyocyaneous  and  the  staphylococcus 
aureus,  and  in  another  case  the  infection  was  due  to  the  anthrax 
bacillus. 

In  most  of  these  cases  the  meningitis  is  secondary  to  infec- 
tion elsewhere,  which  fact  complicates  the  clinical  history 
relating  to  the  meningeal  symptoms. 

Meningitis  Due  to  the  Pneumococcus. 
Judging  from  the  literature,  the  pneumococcus  appears  to  be 
the  organism  most  commonly  associated  with  meningitis.  Not 
only  has  it  been  found  in  most  of  the  sporadic  cases,  but 
extensive  epidemics  are  reported  as  having  been  caused  by  this 
organism.  The  fact  that  the  pneumococcus  organism  was  the  first 
organism  that  wS^s  described  in  connection  with  acute  meningitis, 
and  that  the  first  ^ases  in  which  it  was  found  were  cases  of  menin- 
gitis secondary  to  pneumonia  and  acute  endocarditis,  has  led  to 
this  organism  being  generally  regarded  as  the  cause  even  of 
epidemic  meningitis.  We  have  found  in  our  reports  ten  cases 
in  which  the  pneumococcus  was  found,  and  so  associated  with 
the  lesions  of  the  disease  that  it  can  certainly  be  regarded  as 
the  cause.  In  eight  of  these  cases  the  meningitis  was  secondary. 
In  two  there  was  fracture  of  the  base  of  the  skull,  extending 
across  the  temporal  bone,  the  organism  evidently  gaining  entrance 
into  the  meninges  from  the  middle  ear.  In  one  there  was  otitis 
media  with  necrosis  of  the  bone,  and  the  pneumococci  were 
found  both  in  the  pus  from  the  ear  and  in  the  meninges.  In 
three  the  meningitis  was  secondary  to  acute  croupous  pneumo- 
nia, and  in  one  case  to  acute  fibrinous  pericarditis.  In  one  case 
there  was  broncho-pneumonia  and  thrombosis  of  the  longitudi- 
nal sinus.  In  two  the  affection  of  the  meninges  was  primary, 
no  other  lesions  due  to  the  organism  having  been  found  in  the 
body.  We  regret  to  say  that  in  none  of  these  cases  was  the 
histological  examination  carried  out  so  thoroughly  as  in  the 
epidemic    meningitis.      Only    portions    of    the    brain    cut    from 


167 

various  places  with  the  meninges  attached  were  examined  as  a 
matter  of  routine,  to  confirm  the  anatomical  and  bacteriological 
investigation.  A  thorough  and  systematic  examination  of  the 
nerves  was  not  made.  In  two  cases,  one  of  them  primary  and 
the  other  secondary  to  croupous  pneumonia,  the  sections  and 
portions  of  tissue  were  preserved,  and  from  these  more  detailed 
examinations  have  been  made. 

The  records  of  the  autopsies  show  some  difference  in  the 
description  of  the  amount  and  distribution  of  the  exudation  in  the 
meninges.  In  one  case  secondary  to  acute  croupous  pneumonia 
there  was  only  a  slight  fibrino-purulent  exudation  over  the  base  of 
the  brain  extending  a  short  distance  over  the  lateral  convexity  on 
each  side.  In  another  case  there  was  extensive  exudation  over 
the  base  and  over  almost  the  entire  surface  of  the  brain.  In  but 
one  case  is  it  especially  mentioned  that  the  exudation  extended  in 
lines  along  the  vessels  in  the  sulci,  a  condition  which  was  so 
common  in  the  epidemic  meningitis.  The  exudation  was  usually 
confined  to  the  meshes  of  the  pia  arachnoid,  but  in  one  case  it  is 
said  to  have  been  both  in  the  membranes  and  on  the  surface. 
The  microscopic  examination  showed  considerable  differences  in  the 
lesions  here  as  compared  with  the  epidemic  form.  Fibrin  was 
present  in  the  exudation  in  much  greater  amount.  It  was  found 
both  forming  a  mesh- work  within  which  pus  cells  lay,  and  in 
separate  masses.  The  fibrin  was  generally  in  coarser  filaments  than 
in  the  exudation  in  the  lung  alveoli,  and  in  places  had  undergone 
hyaline  transformation.  Some  of  the  smaller  veins  were  thrombosed 
and  surrounded  by  a  reticulum  of  hyaline  fibrin,  a  condition 
similar  to  that  often  found  in  the  vicinity  of  diphtheritic  mem- 
brane. In  the  specimens  examined  the  exudation  was  confined  to 
the  meshes  of  the  pia-arachnoid,  the  surface  of  the  arachnoid 
being  smooth  and  free  from  change.  The  cells  in  the  exudation 
were  chiefly  polynuclear  leucocytes.  These  were  most  abundant  in 
the  meshes  of  the  fibrin,  and  were  to  some  extent  seen  in  large 
masses  without  any  fibrin  between  them.  Close  to  the  surface 
of  the  brain  and  beneath  the  surface  of  the  arachnoid,  in  addi- 
tion to  the  polynuclear  leucocytes,  there  were  large  numbers  of 
cells  somewhat  larger   than   these,  with  round   vesicular   nuclei. 


168 

None  of  these  contained  pus  cells  in  its  protoplasm.  While  it 
seems  probable  that  these  cells  came  from  a  proliferation  of  the 
connective  tissue  cells  of  the  meninges,  it  was  not  possible  to 
prove  this.  The  large  cells  enclosing  large  numbers  of  leucocytes 
which  were  so  prominent  in  the  exudation  in  epidemic  meningitis 
were  generally  absent.  In  one  of  the  cases  a  few  were  found  on 
the  borders  of  the  masses  of  pus  cells.  The  most  marked  feature 
in  the  process  in  both  the  pneumococcus  and  the  streptococcus 
meningitis  was  the  acute  endarteritis.  This  condition  is  similar  in 
kind  to  the  vascular  lesions  which  have  been  described  in 
tuberculosis  of  the  meninges.  The  condition  of  the  circulation  in 
these  vessels  could  not  be  ascertained.  In  many  of  them  there 
seemed  no  other  change  than  the  acute  inflammation  of  the  wall. 
In  some  the  lumen  was  filled  with  cells,  chiefly  leucocytes,  and  in 
others  there  was  a  mass  of  fibrin  and  red  corpuscles.  The 
inflammatory  change  consisted  essentially  in  an  accumulation  of 
cells  between  the  endothelium,  which  was  generally  elevated  in 
festoons,  and  the  elastic  lamina.  In  some  cases  the  cell 
accumulations  were  so  great  as  to  occlude  the  lumen  of  the  vessels, 
the  endothelial  coat  lying  as  an  irregular  mass  in  the  centre.  In 
others  the  changes  were  so  slight  that  they  might  escape  notice. 
The  endothelium  in  some  places  was  broken  through  and  rolled  up, 
the  cells  then  filling  the  vessel.  The  cells  were  principally  poly- 
nuclear  leucocytes,  and  among  them  some  larger  cells  of  an 
epithelioid  character.  It  was  not  possible  to  ascertain  the 
probable  origin  of  the  larger  cells  in  the  specimens  we  have.  The 
muscularis  in  most  cases  was  unchanged ;  in  others  it  was 
partially  invaded  by  leucocytes.  In  one  case  extensive  lesions 
were  found  in  the  muscularis.  The  vessel  was  greatly  dilated,  the 
muscularis  in  places  apparently  broken  through  or  destroyed,  and 
in  these  places  the  tissue  was  filled  with  leucocytes.  Outside  of 
the  muscularis  there  was  often  considerable  exudation.  In  the 
sections  of  the  meninges  of  the  cord  which  were  examined,  the 
exudation  was  of  the  same  character  as  that  in  the  brain,  but 
more  limited  in  amount.  There  were  but  slight  changes  in  the 
tissues  of  the  brain.  In  one  case  there  seemed  to  be  no  involve- 
ment of  the  cortex,  and  in  the  other  there  was  oedema  and  slight 


169 

softening  of  the  outer  layer  of  the  cortex,  with  some  infiltration 
with  pus  cells.     No  lesions  were  found  in  the  neuroglia. 

The  clinical  histories  in  the  eight  cases  in  which  the  meningitis 
was  secondary  to  other  conditions  do  not  throw  a  great  deal  of 
light  on  the  symptoms  to  be  attributed  to  the  meningitis.  The 
symptoms  referable  to  this  are  complicated  with  symptoms  due  to 
other  lesions.  In  only  four  cases  was  vomiting  present.  Opisthot- 
onos was  found  in  but  one  case,  and  in  this  it  was  slight. 

There  were  few  symptoms  relating  to  the  eyes.  In  one  case,  in 
which  the  meningitis  was  evidently  secondary  to  an  acute  fibrinous 
pericarditis,  there  was  a  hsemorrhagic  eruption  on  the  trunk  and 
limbs  which  appeared  two  days  before  death.  Delirium  was  less 
common  than  in  the  epidemic  cases,  and  in  four  cases  there  was 
unconsciousness.  In  one  of  the  cases  of  pneumonia  in  which  there 
was  an  extensive  exudation  in  the  meninges  there  was  nothing  in 
the  symptoms  which  pointed  to  this. 

In  general  it  may  be  said  that  the  differences  between  the 
clinical  history  of  pneumococcus  meningitis  as  compared  with  the 
epidemic  form  is  in  the  absence  or  slight  development  of  symptoms 
in  the  pneumococcus  form,  which  point  to  extensive  infection  of 
meninges,  of  the  cord  and  spinal  roots,  and  extension  of  the  in- 
fection along  the  cranial  nerves.  At  the  same  time  it  must  be 
remarked  that  our  observations  are  not  sufficiently  numerous  to 
enable  us  to  make  any  extensive  generalizations. 

The  temperature  charts  are  extremely  indefinite.  In  most  cases 
the  patients  were  in  the  hospital  for  such  short  periods  before 
death  that  the  charts  do  not  show  the  course  of  the  disease.  In 
two  of  the  cases  there  w^s  a  terminal  rise  to  107°  and  108°.  The 
temperature  chart  which  is  appended  comes  from  a  patient  who 
entered  the  hospital  with  well-marked  pneumonia  and  a  history  of 
sickness  one  week  before  entry.  The  first  drop  in  the  temperature 
is  probably  that  of  the  crisis  of  pneumonia.  This  was  followed  by 
a  slight  rise,  which  might  be  referred  to  an  extension  of  the 
pneumonia  or  to  the  beginning  infection  of  the  meninges.  On  the 
16th  there  was  vomiting,  and  on  the  17th  active  delirium,  which 
continued  until  unconsciousness  came  on  a  few  hours  before  death. 
At  the  autopsy  there  was  gray  hepatization  in  the  lower  lobe  of 


170 


right  lung,  red  hepatization  in  the  lower  lobe  of  left  lung,  and 
fibrino-purulent  meningitis.  All  of  the  eight  cases  were  in  adults, 
and  the  average  age  was  thirty-four  years. 


Greater  interest   is   attached   to   the   two   cases   in  which  the 
meningitis   was    primary.     In    one    case,   a    well-nourished   and 


171 

well-built  child  of  ten  months,  there  was  a  history  of  slight 
gastro-intestinal  disturbances  two  weeks  before  onset.  The  dis- 
ease began  with  restlessness,  high  fever  (105°  F.)  and  vomiting,  the 
temperature  continuing  high  until  death,  three  days  after  onset. 
The  autopsy  showed  fibrino-purulent  exudation  in  the  meninges 
of  the  brain,  apparently  extending  down  the  cord,  only  the  upper 
portion  of  which  was  removed  with  the  brain.  Pneumococci  with 
well-marked  capsules  were  found  in  the  meninges,  and  cultures 
showed  general  pneumococcus  infection.  (We  are  indebted  to 
Dr.  Wentworth  for  the  clinical  notes  on  this  case.) 

The  other  case  was  that  of  a  child  who  was  taken  when  six 
days  old  with  general  clonic  convulsions,  accompanied  by  a 
temperature  of  104°  in  the  first  twelve  hours,  which  afterwards 
dropped  to  102°.  The  only  symptoms  were  convulsions.  Death 
occurred  on  the  second  day.  The  autopsy  showed  extensive 
exudation  in  the  meninges  of  the  brain  (cord  not  examined) . 
Microscopic  examination  of  the  exudation  showed  numbers  of 
typical  pneumococci.     (Rotch,  "Pediatrics,"  p.  695.) 

Meningitis  Due  to  Streptococcus. 

There  were  eight  cases  of  this,  and  in  all  the  meningitis  was 
secondary  to  infection  elsewhere.  In  four  cases  the  primary 
infection  was  in  the  ear,  and  in  two  of  these  there  was 
thrombosis  of  the  lateral  sinus.  In  one  the  meningitis  repre- 
sented an  extension  to  the  meninges  of  an  erysipelas  of  the 
face  and  scalp.  In  one  case  there  was  acute  endocarditis,  and 
in  one  the  meningitis  was  secondary  to  an  alveolar  abscess.  One 
case  was  of  special  interest,  in  showing  an  infection  which  doubt- 
less took  place  from  the  nose.  In  this  case  there  was  fracture 
of  the  base  of  the  skull,  extending  across  the  cribiform  plate  of 
the  ethmoid  bone.  Pus  and  abundant  streptococci  were  found 
in  the  nose. 

In  these  cases  the  lesions  in  the  meninges  were  very  similar  to 
those  found  in  the  pneumococcus  infection.  The  exudation  was 
purulent,  with  a  variable  amount  of  fibrin,  usually  not  so  much 
as  in  the  pneumococcus  cases.  The  acute  endarteritis  was  well 
marked,  and  there  was  no  extension  of  the  process  into  the  brain. 


172 

The  organisms  were  found  in  large  numbers  in  the  exudation. 
The  clinical  histories  of  all  these  cases  do  not  show  anything  of 
especial  importance.  Opisthotonos  was  found  in  but  one. case, 
and  was  not  well  marked.  Pain  and  stiffness  of  the  neck  were 
found  in  two  cases.  Symptoms  referable  to  the  eyes  were  noted 
in  three  cases. 

Tubercular  Meningitis. 

Twelve  cases  of  tuberculous  meningitis  were  found.  Tuber- 
culosis of  the  meninges  in  general  presents  a  different  anatomical 
picture  from  tuberculosis  elsewhere  in  the  body,  in  the  extent 
of  the  acute  inflammatory  lesions  with  fibrino-purulent  exudation, 
which  accompanies  the  formation  of  tubercles  and  tuberculous 
tissue.  This,  though  present  to  some  extent  in  tuberculous 
lesions  elsewhere,  never  reaches  the  same  extent  as  in  the  brain. 

We  shall  not  enter  into  a  more  detailed  description  of  the 
clinical  and  anatomical  features  of  this  form  of  meningitis, 
which  is  perhaps  the  best  known  of  all. 

Anthrax  Meningitis. 

The  case  is  that  of  a  man  about  forty  years  of  age,  a 
teamster,  engaged  in  handling  hides.  He  had  a  carbuncle  in 
the  neck,  which  was  removed  by  operation.  Infection  of  the 
alimentary  canal  probably  took  place  through  the  instrumentality 
of  his  fingers,  which  he  was  constantly  putting  into  his  mouth 
to  feel  an  inflamed  tooth.  At  the  autopsy  there  were  thirteen 
carbuncles  in  various  places  in  the  intestinal  canal,  and  an 
acute  hsemorrhagic  meningitis  with  focal  haemorrhages  through- 
out the  brain.  The  exudation  in  the  meninges  was  distinctly 
hsemorrhagic,  and  numerous  anthrax  bacilli  were  found  in  the 
tissues. 

There  is  no  doubt  that  acute  meningitis  may  be  produced  by 
the  entrance  into  the  meninges  of  a  number  of  infectious 
organisms.  These  forms  are  rarely  primary.  The  organisms 
enter  the  meninges  either  by  the  formation  of  a  communication 
between  the  meninges  and  some  cavity  where  they  may  be 
accidentally  present  (as  in  the  middle  ear  or  nose),  or  by  the  ex- 


173 

tension  to  the  meninges  of  an  infectious  process  in  the  vicinity 
(mastoiditis,  erysipehxs),  or  they  are  brought  to  the  meninges  by 
the  blood  from  some  other  focus  in  the  body  (pneumonia, 
endocarditis).  In  tuberculous  meningitis  we  have  never  found 
a  single  case  in  which  the  lesions  in  the  meninges  could  be 
regarded  as  primary.  The  only  two  cases  of  apparently  primary 
infection  were  in  the  two  pneumococcus  noted,  and  in  one  of 
these  the  infection  may  have  come  from  the  intestinal  canal. 
We  believe  that  all  infections  of  the  meninges  other  than  the 
diplococcus  intracellularis  are  fatal,  but  this  can  only  be  deter- 
mined by  microscopic  and  bacteriological  examination  of  the 
exudation  obtained  during  life  by  spinal  puncture.  If  tubercle 
bacilli,  pneumococci  or  streptococci  are  found  with  the  evidences 
of  meningitis  in  a  case  which  recovers,  it  would  settle  the  point ; 
clinical  evidence,  without  lumbar  puncture,  will  not. 


174 


DESCRIPTION  OF  PLATES. 


Plate  1 :  — 

Fig.  1.  Forty-eight-hour  culture  of  diplococcus  intracellulains  on 
Loefifler's  blood-serum  mixture. 

Fig.  2.  Abundant  growth  in  twenty-four-hour  culture  on  fresh  blood- 
serum.  The  colonies  are  minute,  very  numerous,  and 
somewhat  resemble  similar  cultures  of  the  pneumococcus. 

Plate  2 :  — 
Fig.  1.     Portion   of    the  surface  of  the  brain  from  case  of  five  days 
duration. 

Fig.  2.    Posterior  surface  of  lumbar  cord  from  the  same  case. 

Fig.  3.  Portion  of  surface  of  brain  from  a  case  of  seventy-four  days' 
duration. 

Plate  3:  — 
Fig.  1.  Pus  cells  containing  diplococci  from  the  meninges.  A  few 
diplococci  are  in  the  exudate  outside  of  the  pus  cells. 
Between  the  pus  cells  there  are  delicate  fibrillse  of  fibrin. 
The  drawing  is  an  accurate  representation  of  a  group  of 
cells  in  the  field  of  the  microscope. 

Fig.  2.  Pus  cells  from  an  alveolus  of  the  lung  in  a  case  of  diplococcus 
pneumonia.  The  cells  are  swollen,  and  contain  immense 
numbers  of  diplococci. 

Fig.  3.  Section  passing  through  a  sulcus  in  brain  of  goat  which  died  of 
experimental  meningitis.  The  exudation  extends  into  the 
cortex,  and  there  are  pus  cells  both  around  the  vessels  and 
infiltrating  the  tissue. 

Plate  4:  — 
Fig.  1.     Cross-section  of  optic  nei've  close  to  eye,  showing  the  purulent 
infiltration  of  the  inner  sheath  of  the  nerve  in  places  ex- 
tending between  the  nerve  bundles. 

Fig.  2.  Cross-section  of  the  posterior  root  of  lower  dorsal  cord  from 
an  acute  case,  showing  hyperaemia  and  purulent  infiltra 
tion  of  nerve. 


175 

Plate  5 : — 

Fig.  1.  Longitudinal  section  of  auditory  nerve  in  acute  case,  showing 
purulent  infiltration  in  and  around  the  nerve. 

Fig.  2.  Section  of  edge  of  Gasserian  ganglion  from  acute  ease,  show- 
ing purulent  infiltration  of  nerve  and  ganglion. 

Plate  6:  — 

Fig.  1.  Section  of  posterior  root  ganglion  of  cervical  cord,  showing 
purulent  infiltration  with  degeneration  of  ganglion  cells. 

Fig.  2.  Portion  of  meninges  in  acute  case,  showing  the  formation  of 
large  epithelioid  cells.  The  cells  lying  free  enclose  poly- 
nuclear  leucocytes.     Immersion, 

Plate  7 :  — 
Fig.  1.     Section  of  posterior  root  from  chronic  case,  showing  perivas- 
cular infiltration.     The  plasma  and  lymphoid  cells  are  the 
most  numerous.     The  cells  with  deep-blue  protoplasm  are 
plasma  cells.     Immersion. 

Figs.  2,  3,  4,  Sections  showing  neuroglia  proliferation :  Fig.  2,  neu- 
roglia cell  from  olfactory  nerve,  showing  nuclear  figure ; 
Fig.  3,  same  fi*om  optic  nerve  from  acute  case;  Fig.  4, 
large  neuroglia  cells,  some  with  numerous  nuclei  from 
beneath  lateral  ventricle  in  case  of  fourteen  days'  duration. 
Immersion. 

Plate  8:  — 
Fig.  1.     Section  of  posterior  nerve  root,  showing  degeneration.     (On 
the  right  the  nerve  has  been  slightly  crushed  in  cutting.) 
Marchi  method. 

Fig.  2.  Section  of  optic  nerve  from  same  case  as  Plate  4,  Fig.  1,  show- 
ins:  desreneration.     Marchi  method. 


176 


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MASS.   STATE    BOARD    OF    HEALTH. 


PLATE    No. 


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F.   Byrnes,  del. 


HELtOTYPE  PTG.   CO.    3QST0N 


CEREBRO    SPINAL    MENINGITIS. 

[  Councilman.] 


MASS.   STATE    BOARD    OF    HEALTH. 


PLATE    No.   2. 


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CEREBRO    SPINAL    MENINGITIS. 
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MASS.   STATE    BOARD    OF    HEALTH. 


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